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  • Article

    Levetiracetam inhibits THP-1 monocyte chemotaxis and adhesion via the synaptic vesicle 2A (Retracted Article)

    Authors
    Zhang, Yue; Hu, Min; Tang, Yue-yu; Zhang, Bei; Han, Yin-yin; Huang, Zheng-yu; Chen, Chen; Li, Gang
    Part of
    Biochemical and biophysical research communications, 2020-04, Vol.525 (1), p.14-19
    Abstract
    • Long-term therapy with older antiepileptic drugs (AEDs), but not levetiracetam (LEV), may increase the risk of atherosclerosis (AS), suggesting that LEV may have a potential anti-AS effect. The synaptic vesicle 2A (SV2A) is known to the specific binding site of LEV. Numerous studies have documented that SV2A is a membrane protein specifically expressed in nervous system. Interestingly, our previous research showed that SV2A also existed in human CD8(+) T lymphocytes. Therefore, we hypothesized that LEV was associated with decreased risk of AS by regulating monocytes chemotaxis and adhesion. We showed that SV2A protein were detected in THP-1 human monocytic leukemia cells. LEV (300 mu M) inhibited the chemotaxis and adhesion of THP-1 cells after transfection with plasmids expressing SV2A(WT), but not SV2A(R383Q) which was a known functional mutation site of human SV2A. Furthermore, RT-PCR and western blot analysis demonstrated that LEV (300 mM) decreased the expression level of chemokine-related receptors (CX3CL1, CCR1, CCR2, and CCR5),and reduced levels of phosphorylated AKT (p-AKT) in THP-1 cells with SV2AWT expressing plasmids. Taken together, these findings indicated that LEV has an inhibitory effect on THP-1 monocyte adhesion and chemotaxis, suggesting that SV2A may serve as a novel therapeutic target to prevent AS. (C) 2020 Elsevier Inc. All rights reserved.
    Subjects
    Biochemistry & Molecular Biology; Biophysics; Life Sciences & Biomedicine; Science & Technology
  • Article

    Okadaic acid promotes epithelial‐mesenchymal transition of hepatocellular carcinoma cells by inhibiting protein phosphatase 2A

    Authors
    Kong, Juan; Li, Di; Zhang, Shidong; Zhang, Huixia; Fu, Yuanyuan; Qian, Bo; Bei, Chunhua; Tan, Shengkui; Zhu, Xiaonian
    Part of
    Journal of cellular biochemistry, 2021-09, Vol.122 (9), p.993-1002
    Abstract
    • As a specific inhibitor of serine/threonine protein phosphatases, okadaic acid (OA) has been found to be a tumor promoter. However, whether OA plays a role in metastasis of hepatocellular carcinoma (HCC) has not been well elucidated. In this study, Hep3B and HepG2 cells were treated with different doses of OA and the cell viability was determined by CCK8 test. As a result, Hep3B and HepG2 cells showed no obvious cytotoxicity after OA treatment below 20 or 25 nM for 12 or 24 hours. However, wound healing, invasion, and migration abilities of HCC cells were significantly enhanced in the OA‐treated groups than those of the control group (P < .05), measured by cell scratching and BD transwell assays. Moreover, we found that the expression of epithelial‐mesenchymal transition (EMT)‐related key factors was changed upon OA treatment in a dose‐dependent manner. In addition, the activity of protein phosphatase 2A (PP2A) in OA‐treated cells was also decreased significantly compared with the control cells (P < .05). Interfering of PP2A subunit A or C caused a similar expression change of EMT‐related key factors as the OA treatment in HCC cells. Our results suggest that OA promotes the EMT process of HCC cells by inhibiting the activity of PP2A. We report a novel role of okadaic acid (OA) in hepatocellular carcinoma metastasis, and explore a mechanism of OA in inducing epithelial‐mesenchymal transition process via inhibiting the activity of PP2A.
    Subjects
    EMT; HCC; metastasis; PP2A
  • Article

    Activation of Protein Phosphatase 2A by Palmitate Inhibits AMP-activated Protein Kinase

    Authors
    Wu, Yong; Song, Ping; Xu, Jian; Zhang, Miao; Zou, Ming-Hui
    Part of
    Journal of Biological Chemistry, 2007-03, Vol.282 (13), p.9777-9788
    Abstract
    • Elevated levels of free fatty acids contribute to cardiovascular diseases, but the mechanisms remain poorly understood. The present study was aimed to determine if free fatty acid inhibits the AMP-activated kinase (AMPK). Exposure of cultured bovine aortic endothelial cells (BAECs) to palmitate (0.4 mm) but not to palmitoleic or oleic acid (0.4 mm) for 40 h significantly reduced the Thr172 phosphorylation of AMPK-α without altering its protein expression or the phosphorylation of LKB1-Ser428, a major AMPK kinase in BAECs. Further, in LKB1-deficient cells, palmitate suppressed AMPK-Thr172 implying that the inhibitory effects of palmitate on AMPK might be independent of LKB1. In contrast, 2-bromopalmitate, a non-metabolizable analog of palmitate, did not alter the phosphorylation of AMPK and acetyl-CoA carboxylase. Further, palmitate significantly increased the activity of protein phosphatase (PP)2A. Inhibition of PP2A with either okadaic acid, a selective PP2A inhibitor, or PP2A small interference RNA abolished palmitate-induced inhibition on AMPK-Thr172 phosphorylation. Exposure of BAECs to C2-ceramide, a cell-permeable analog of ceramide, mimicked the effects of palmitate. Conversely, fumonisin B1, which selectively inhibits ceramide synthase and decreases de novo formation of ceramide, abolished the effects of palmitate on both PP2A and AMPK. Inhibition of AMPK in parallel with increased PP2A activity was founded in C57BL/6J mice fed with high fat diet (HFD) rich in palmitate but not in mice fed with HFD rich in oleate. Moreover, inhibition of PP2A with PP2A-specific siRNA but not scrambled siRNA reversed HFD-induced inhibition on the phosphorylation of AMPK-Thr172 and endothelial nitric-oxide synthase (eNOS)-Ser1177 in mice fed with high fat diets. Taken together, we conclude that palmitate inhibits the phosphorylation of both AMPK and endothelial nitric-oxide synthase in endothelial cells via ceramide-dependent PP2A activation.
    Subjects
    AMP-Activated Protein Kinases; Animals; Biochemistry; Cattle; Cell Biology; Cell Line; Enzyme Activation - physiology; Enzyme Activators - pharmacology; HeLa Cells; Humans; Male; Mice; Mice, Inbred C57BL; Molecular Biology; Multienzyme Complexes - antagonists & inhibitors; Nitric Oxide Synthase Type III - antagonists & inhibitors; Palmitates - pharmacology; Phosphoprotein Phosphatases - metabolism; Phosphoprotein Phosphatases - physiology; Phosphorylation; Protein Phosphatase 2; Protein-Serine-Threonine Kinases - antagonists & inhibitors
  • Article

    The Overexpression of Kinesin Superfamily Protein 2A (KIF2A) was Associated with the Proliferation and Prognosis of Esophageal Squamous Cell Carcinoma (Retracted article. See vol. 14, pg. 981, 2022)

    Authors
    Li, Demao; Sun, Huijie; Meng, Linglei; Li, Deshang
    Part of
    Cancer management and research, 2020-01, Vol.12, p.3721-3729
    Abstract
    • Aim: Kinesin family member 2A (KIF2A) is a member of the kinesin-13 superfamily protein. KIF2A played a role in the development of many tumors. However, the role of KIF2A in esophageal squamous cell carcinoma (ESCC) remains unclear. In this study, we aimed to investigate the role of KIF2A in ESCC. Methods: We used bioinformatics analysis to study the expression levels and prognosis of KIF2A in ESCC and normal tissues. We also used our own samples to verify the results by immunohistochemistry. Then, the biological functions of KIF2A in ESCC was studied by cell experiments and animal experiments. Results: Both the TCGA database and our samples showed that KIF2A was relatively highly expressed in ESCC tissues and was significantly associated with disease-free survival (P =0.037) in TCGA database. Colony formation assay, CCK8 and Western blotting results showed that knockdown of KIF2A can significantly reduce colony forming ability and proliferation ability. The results of animal experiments showed that knocking down KIF2A can significantly reduce the tumor volume of mice. Conclusion: KIF2A might be used as a prognostic factor for ESCC, and knockdown of KIF2A could inhibit ESCC proliferation in vitro and in vivo, respectively. KIF2A could serve as a potential prognostic biomarker and therapeutic target for future ESCC.
    Subjects
    Analysis; Animal experimentation; escc; Esophageal cancer; esophageal squamous cell carcinoma; Immunohistochemistry; kif2a; Kinesin; kinesin superfamily protein 2a; Life Sciences & Biomedicine; Oncology; Original Research; Prognosis; proliferation; Science & Technology; Squamous cell carcinoma
  • Article

    RETRACTED: Okadaic acid promotes epithelial‐mesenchymal transition of hepatocellular carcinoma cells by inhibiting protein phosphatase 2A

    Authors
    Kong, Juan; Li, Di; Zhang, Shidong; Zhang, Huixia; Fu, Yuanyuan; Qian, Bo; Bei, Chunhua; Tan, Shengkui; Zhu, Xiaonian
    Part of
    Journal of cellular biochemistry, 2021-09, Vol.122 (9), p.993-1002
    Abstract
    • As a specific inhibitor of serine/threonine protein phosphatases, okadaic acid (OA) has been found to be a tumor promoter. However, whether OA plays a role in metastasis of hepatocellular carcinoma (HCC) has not been well elucidated. In this study, Hep3B and HepG2 cells were treated with different doses of OA and the cell viability was determined by CCK8 test. As a result, Hep3B and HepG2 cells showed no obvious cytotoxicity after OA treatment below 20 or 25 nM for 12 or 24 hours. However, wound healing, invasion, and migration abilities of HCC cells were significantly enhanced in the OA‐treated groups than those of the control group (P < .05), measured by cell scratching and BD transwell assays. Moreover, we found that the expression of epithelial‐mesenchymal transition (EMT)‐related key factors was changed upon OA treatment in a dose‐dependent manner. In addition, the activity of protein phosphatase 2A (PP2A) in OA‐treated cells was also decreased significantly compared with the control cells (P < .05). Interfering of PP2A subunit A or C caused a similar expression change of EMT‐related key factors as the OA treatment in HCC cells. Our results suggest that OA promotes the EMT process of HCC cells by inhibiting the activity of PP2A.
    Subjects
    Cell migration; Cell viability; Cytotoxicity; Hepatocellular carcinoma; Liver cancer; Mesenchyme; Metastases; Okadaic acid; Phosphatase; Phosphoprotein phosphatase; Protein phosphatase; Proteins; Scratching; Serine; Threonine; Toxicity; Wound healing
  • Article

    RETRACTED: Allosteric Activators of Protein Phosphatase 2A Display Broad Antitumor Activity Mediated by Dephosphorylation of MYBL2

    Authors
    Morita, Ken; He, Shuning; Nowak, Radosław P.; Wang, Jinhua; Zimmerman, Mark W.; Fu, Cong; Durbin, Adam D.; Martel, Megan W.; Prutsch, Nicole; Gray, Nathanael S.; Fischer, Eric S.; Look, A. Thomas
    Part of
    Cell, 2020-04, Vol.181 (3), p.702-715.e20
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the authors. Their study showed that different PP2A holoenzymes, composed of distinct subunits and acting on unique substrates, can be specifically targeted by different small-molecule allosteric activators, including perphenazine. An important part of the study was the identification of a compound the authors called iHAP1 (improved heterocyclic activator of PP2A) that was suitable for in vivo studies in zebrafish and murine models because it did not interfere with dopamine signaling, which caused dose limiting off-target toxicity in the case of perphenazine. The authors also assessed iHAP1 for a second type of off-target activity involving inhibition of tubulin polymerization, and they reported that iHAP1 did not affect tubulin polymerization into microtubules (Figures S6D and S6E). Recently, Vit and coworkers published an article in The EMBO Journal showing that iHAP1 does in fact significantly inhibit tubulin polymerization (Vit et al., 2022, EMBO J. 41, e110611, https://doi.org/10.15252/embj.2022110611). The authors have subsequently used the same tubulin polymerization kit that they originally used for determining the effects of small molecules on the rate of tubulin polymerization and carefully optimized the conditions with the control compounds provided with the kit. After recalibration of the plate reader based on these controls, the authors determined that their original results are not reproducible and that iHAP1 does in fact potently inhibit tubulin polymerization. They are uncertain why their original analysis yielded inaccurate results. Unfortunately, the fact that iHAP1 inhibits tubulin polymerization renders uninterpretable their in vivo studies showing anti-cancer cell activity in zebrafish and murine models, because they cannot tell how much of the activity is due to activation of PP2A and how much is contributed by the anti-tubulin activities of this molecule. Because these in vivo studies and other in vitro studies in the paper prominently include iHAP1, all of the authors have agreed that the most appropriate course of action is to retract the paper. Many in vitro experiments in the paper that address different aspects of PP2A activation were performed with both iHAP1 and perphenazine, which does not possess detectable anti-tubulin activity. In view of the error involving iHAP1 and anti-tubulin polymerization, the authors are currently repeating each of these experiments in the original article in Cell; however, this will take a much longer time. They have decided the most responsible thing is to retract the paper now, so that others are not led to perform uninterpretable experiments with the iHAP1 compound. The authors regret and apologize for this mistake.
    Subjects
    Apoptosis; Cell Cycle Proteins - drug effects; Cell Cycle Proteins - metabolism; Cell Line, Tumor; Enzyme Activators - metabolism; G1 Phase; General Biochemistry, Genetics and Molecular Biology; Humans; Multiprotein Complexes - metabolism; Multiprotein Complexes - physiology; Phenothiazines - pharmacology; Phosphorylation; Protein Phosphatase 2 - metabolism; Protein Phosphatase 2 - physiology; Protein Subunits - metabolism; Trans-Activators - drug effects; Trans-Activators - metabolism; Transcription Factors - metabolism
  • Article

    RETRACTED: Levetiracetam inhibits THP-1 monocyte chemotaxis and adhesion via the synaptic vesicle 2A

    Authors
    Zhang, Yue; Hu, Min; Tang, Yue-yu; Zhang, Bei; Han, Yin-yin; Huang, Zheng-yu; Chen, Chen; Li, Gang
    Part of
    Biochemical and biophysical research communications, 2020-04, Vol.525 (1), p.14-19
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the authors. The authors had found some conflicted results of the CCR1 protein expression level, which was showed in the Fig.4D, in the latest experiments after the submission. After careful discussion of all authors, the authors thought current results might be too preliminary to draw a conclusion and further rigorous and careful research had to be carried out. Therefore, all of the authors have agreed to retract this article. The authors deeply apologized for this error and any potentially misleading to the journal readers.
  • Article

    Outer Membrane Protein A (OmpA) of Shigella flexneri 2a Links Innate and Adaptive Immunity in a TLR2-dependent Manner and Involvement of IL-12 and Nitric Oxide

    Authors
    Pore, Debasis; Mahata, Nibedita; Chakrabarti, Manoj K.
    Part of
    Journal of Biological Chemistry, 2012-04, Vol.287 (15), p.12589-12601
    Abstract
    • We determine that OmpA of Shigella flexneri 2a is recognized by TLR2 and consequently mediates the release of proinflammatory cytokines and activates NF-κB in HEK 293 cells transfected with TLR2. We also observe that in RAW macrophages TLR2 is essential to instigate the early immune response to OmpA via NF-κB activation and secretion of cytokines and NO. Consistent with these results, TLR2 knockdown using siRNA abolishes the initiation of immune responses. Processing and presentation of OmpA depend on TLR2; MHCII presentation of the processed antigen and expression of CD80 significantly attenuated in TLR2 knockdown macrophages. The optimum production of IFN-γ by the macrophages:CD4+ T cells co-culture depends on both TLR2 activation and antigen presentation. So, TLR2 is clearly recognized as a decisive factor in initiating host innate immune response to OmpA for the development of CD4+ T cell adaptive response. Furthermore, we demonstrate in vivo that intranasal immunization of mice with OmpA selectively enhances the release of IFN-γ and IL-2 by CD4+ T cells. Importantly, OmpA increases the level of IFN-γ production in Ag-primed splenocytes. The addition of neutralizing anti-IL-12p70 mAb to cell cultures results in the decreased release of OmpA-enhanced IFN-γ by Ag-primed splenocytes. Moreover, coincubation with OmpA-pretreated macrophages enhances the production of IFN-γ by OmpA-primed CD4+ T cells, representing that OmpA may enhance IFN-γ expression in CD4+ T cells through the induction of IL-12 production in macrophages. These results demonstrate that S. flexneri 2a OmpA may play a critical role in the development of Th1 skewed adaptive immune response. Background: OmpA activates innate immunity through TLR2, but its function and mechanism of targeting adaptive immunity remains unexplored. Results: TLR2 regulates OmpA processing and presentation, NO and cytokine release, which contributes to development of type-1 adaptive immunity. Conclusion: TLR2 is crucial to link innate and adaptive responses stimulated by OmpA. Significance:S. flexneri 2a OmpA, a novel molecule, coordinates the innate and adaptive responses.
    Subjects
    Adaptive Immunity; Animals; Antigen Presentation; Bacterial Outer Membrane Proteins - immunology; Biochemistry; Cell Biology; Cytokine; Enzyme Activation; Female; Flow Cytometry; HEK293 Cells; Histocompatibility Antigens Class II - genetics; Histocompatibility Antigens Class II - metabolism; Host-Pathogen Interactions; Humans; IFN-γ; Immunity, Innate; Immunology; Interferon-gamma - biosynthesis; Interleukin-12 - metabolism; Interleukin-12 - physiology; Interleukin-12 Receptor beta 2 Subunit - genetics; Interleukin-12 Receptor beta 2 Subunit - metabolism; Lymphocyte Activation; Macrophages - enzymology; Macrophages - immunology; Macrophages - metabolism; Mice; Mice, Inbred BALB C; Molecular Biology; NF-kappa B - metabolism; Nitric Oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - metabolism; Outer Membrane Protein A; Phosphorylation; Protein kinase C (PKC); Protein Kinase C-alpha - metabolism; Protein Transport; Receptors, Chemokine - metabolism; Shigella flexneri - immunology; Shigella flexneri - physiology; Shigella flexneri 2a; T-Lymphocytes - immunology; T-Lymphocytes - metabolism; Th1 Response; TLR2; Toll-Like Receptor 2 - genetics; Toll-Like Receptor 2 - metabolism; Toll-Like Receptor 2 - physiology
  • Article

    Long non‐coding RNA ASBEL promotes osteosarcoma cell proliferation, migration, and invasion by regulating microRNA‐21

    Authors
    Zhao, Jianhui; Zhang, Chao; Gao, Zhongli; Wu, Han; Gu, Rui; Jiang, Rui
    Part of
    Journal of cellular biochemistry, 2018-08, Vol.119 (8), p.6461-6469
    Abstract
    • Osteosarcoma is the most common malignant bone tumor in children and adolescents with high rate of incidence, high frequency of recurrence, and high degree of metastasis. This study aimed to investigate the effects of long noncoding RNA antisense ncRNA in the abundant in neuroepithelium area (ANA)/B‐cell translocation gene 3 (BTG3) locus (lncRNA ASBEL) on the pathogenesis of osteosarcoma. The expression levels of ASBEL in human osteoblast cells and human osteosarcoma cells were evaluated using qRT‐PCR. Effects of ASBEL knockdown on cell viability, migration, and invasion were detected using trypan blue exclusion assay, cell migration, and cell invasion assay, respectively. The regulatory effects of ASBEL on microRNA‐21 (miR‐21) were analyzed using qRT‐PCR. The roles of miR‐21 and protein phosphatase 2A (PP2A), the possible downstream factor of miR‐21, in osteosarcoma cell proliferation, migration, and invasion were also explored. The results showed that ASBEL was highly expressed in osteosarcoma cells. Knockdown of ASBEL inhibited osteosarcoma cell viability, migration, and invasion, as well as the expression level of miR‐21. PP2A was a direct target of miR‐21, which participated in the effects of ASBEL and miR‐21 on the activation of phosphatidylinositol 3‐kinase/protein kinase 3/glycogen synthase kinase‐3β (PI3K/AKT/GSK3β) and mitogen‐activated protein kinase/extracellular regulated protein kinase (MEK/ERK) signaling pathways as well as the enhancement of osteosarcoma cell proliferation, migration, and invasion. In conclusion, we verified that ASBEL‐miR‐21‐PP2A pathway might play critical regulatory effects on the pathogenesis of osteosarcoma and could be as the potential therapeutic target and biomarker for osteosarcoma treatment. ASBEL was highly expressed in osteosarcoma cells. Knockdown of ASBEL inhibited osteosarcoma cell viability, migration, and invasion, as well as the expression level of miR‐21. PP2A was a direct target of miR‐21, which was participated in the effects of ASBEL and miR‐21 on the activation of phosphatidylinositol 3‐kinase/protein kinase 3/glycogen synthase kinase‐3β (PI3K/AKT/GSK3β) and mitogen‐activated protein kinase/extracellular regulated protein kinase (MEK/ERK) signaling pathways as well as the enhancement of osteosarcoma cell proliferation, migration, and invasion.
    Subjects
    Bone Neoplasms - genetics; Bone Neoplasms - metabolism; Bone Neoplasms - pathology; Cell Line, Tumor; Cell Movement; Cell Proliferation; Humans; long non‐coding RNA ASBEL; MEK/ERK; MicroRNAs - genetics; MicroRNAs - metabolism; microRNA‐21; Neoplasm Invasiveness; Neoplasm Proteins - genetics; Neoplasm Proteins - metabolism; osteosarcoma; Osteosarcoma - genetics; Osteosarcoma - metabolism; Osteosarcoma - pathology; PI3K/AKT/GSK3β; protein phosphatase 2A; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; RNA, Neoplasm - genetics; RNA, Neoplasm - metabolism; Signal Transduction
  • Article

    Over-expression of HDAC8 down-regulate CDKN2A is associated with worse prognosis of esophageal squamous cell carcinoma (Retracted Article)

    Authors
    Nesa, Effat Un; Chen, Xuan; Wang, Cong; Chen, Xue; Wang, Yuan; Qu, Yan; Mi, Si; Guan, Shanghai; Xiao, Fengxia; Cheng, Yufeng
    Part of
    Translational cancer research, 2020-03, Vol.9 (3), p.1406-1417
    Abstract
    • Background: The epigenetic alteration has an impact on cancer cell cycle regulation. Expression of histone deacetylase 8 (HDAC8) ruled out the expression of cyclin-dependent kinase inhibitor 2A (CDKN2A) and this is linked with the prognosis of Esophageal cancer (EC) patients. Methods: By the immunohistochemical staining, we examined the expression status of HDAC8 and CDKN2A protein of 110 esophageal squamous cell carcinoma (ESCC) patients in the tissue microarray. The nuclear staining intensity was counted by immunoreactivity scoring ranging from 0 to 12 and grouped them into two; weak or non-expression and over-expression. Results: The median follow-up duration of our study was 71 months postoperatively. Up-regulation of HDAC8 expression and down-regulation of CDKN2A (p16) indicate decreased 5-year overall survival (OS) (P=0.003) and (P=0.001) respectively and progression-free survival (PFS) (P=0.005, P=0.001) respectively, which are statistically significant and determined by Kaplan-Meier estimates using log-rank test. Consequently, HDAC8 and CDKN2A act as an independent prognostic biomarker, for OS and PFS that analyzed by multivariate cox-regression analysis, HR 1.173 with 95% CI: 0.215-6.416 and P=0.003 and HR 1.217 with 95% CI: 0.224-6.600 and P=0.005 respectively. Spearman rank test establish the negative correlation between HDAC8 and CDKN2A. Conclusions: Over-expression of HDAC8 and weak or no expression of CDKN2A have a worse impact on EC patients and indicate poor survival and progression of the disease and act as a promising prognostic parameter.
    Subjects
    Life Sciences & Biomedicine; Oncology; Original; Science & Technology
  • Article

    Clinical Efficacy of PEG-IFNα-2a and PEG-IFNα-2b in the Treatment of Hepatitis B e Antigen-Positive Hepatitis B and Their Value in Improving Inflammatory Factors and Hemodynamics in Patients: A Comparative Study

    Authors
    Jia, Nina; Gao, Wei; Fan, Xiaohong; Gao, Hong; Li, Xueqing; Mi, Biantao; Yang, Jie
    Part of
    Oxidative medicine and cellular longevity, 2022, Vol.2022, p.3185320-10
    Abstract
    • Objective. To compare the merits and demerits of PEG-IFNα-2a and PEG-IFNα-2b for the treatment of hepatitis B e antigen (HBeAg)-positive chronic hepatitis B (CHB). Methods. Clinical files from eighty-four CHB patients admitted to the Second Hospital of Shanxi Medical University between January 2018 and January 2019 were retrospectively analyzed and assigned to two groups: group 2a treated with PEG-IFNα-2a and group 2b treated with PEG-IFNα-2b. The clinical efficacy was compared between the above two arms, and the liver function (ALT, AST, HA, LN, and IV-C), HBV-DNA, HBsAg, HBeAg, and inflammatory factors (IFs, IL-1β, IL-6, IL-8, and TNF-α) were tested at 12 weeks (T1), 24 weeks (T2), and 48 weeks (T3). The alterations of hemodynamics (SBP, DBP, MAP, and CVP), cardiac function (LVEF and BNP), and the incidence of adverse reactions (ARs) during treatment were recorded. Finally, the patients were followed up for 2 years to investigate the quality of life (QOL) as well as the positive seroconversion rate of HBsAg and HBeAg. Results. The overall response rate was similar in the two arms (P>0.05). After treatment, the liver function, HBV-DNA, HBsAg, HBeAg, IFs, hemodynamics, and cardiac function were enormously improved (P<0.05), with faster improvement in group 2b compared with group 2a (P<0.05). The investigation of ARs identified notably lower incidence rates of alopecia, thrombocytopenia, and granulocytopenia in group 2a as compared to group 2b (P<0.05). The prognostic follow-up results revealed no distinct difference in the QOL score and the positive seroconversion rate of HBsAg and HBeAg (P>0.05); however, the quantitative results of HBV-DNA, HBsAg, and HBeAg in group 2b were lower than those in group 2a (P<0.05). Conclusions. Both PEG-IFNα-2a and PEG-IFNα-2b have excellent and stable therapeutic effects on HBeAg-positive CHB, among which PEG-IFNα-2b renders a faster treatment process but higher side effects, which can provide valuable references when choosing a treatment plan for CHB.
    Subjects
    Anorexia; Antigens; Antiviral Agents - therapeutic use; Blood pressure; Deoxyribonucleic acid; DNA; DNA, Viral; Hemodynamics; Hepatitis B; Hepatitis B e Antigens; Hepatitis B Surface Antigens; Hepatitis B, Chronic - drug therapy; Hospitals; Humans; Infections; Interferon alpha-2 - therapeutic use; Interferon-alpha; Liver; Polyethylene Glycols; Quality of Life; Recombinant Proteins - therapeutic use; Retrospective Studies; Statistical analysis; Treatment Outcome; Viruses
  • Article

    HPV-16 Expression and Loss of Cell Differentiation in Primary Bladder Tumors

    Authors
    Pang, Lei; Ding, Zijun; Li, Fei; Chai, Hongqiang; Wu, Ming; Shao, Jinkai
    Part of
    BioMed research international, 2022-10, Vol.2022, p.6565620-6
    Abstract
    • Objective. Primary bladder tumors have a high degree of malignancy. To investigate the expression of human papillomavirus type 16 (HPV-16) in primary bladder tumors and the loss of cell differentiation and to explore the significance of HPV-16 detection, it is expected to be a disease. Treatment provides a theoretical basis. Methods. Fifty-seven patients with primary bladder tumors admitted to our hospital from January 2019 to January 2022 were selected as the research subjects, and they were divided into HPV-related groups according to the human papillomavirus (HPV) infection status (n=28) and HPV unrelated group (n=29). The general data of patients were collected, the expression of HPV-16 in bladder tissue samples was detected, and the correlation between pathological parameters and HPV-16 expression was analyzed. Results. Among HPV subtypes, HPV 16 subtype accounted for the highest proportion, followed by HPV-18 and HPV-6 subtypes; there was no significant difference in tumor stage (stage 1, stage a, stage 2a) between the HPV-related group and the HPV-unrelated group (stage 1, stage a, and stage 2a). P>0.05); there was no significant difference in postoperative pathological expression (high expression and low expression) of patients (P>0.05); there was no statistical difference in age and gender between HPV-related and HPV-unrelated groups (P>0.05), HPV-related group and HPV-unrelated group compared daily regular drinking and smoking status, the difference was statistically significant (P<0.05); HPV-16 expression was not correlated with tumor differentiation degree and age of patients (P>0.05); the area under the curve (AUC) of HPV-16 for judging primary bladder tumor expression and cellular molecular deletion was 0.891, with a sensitivity of 83.94% and a specificity of 88.57%. Conclusion. HPV-16 is an upper, expressed in primary bladder tumors and will participate in the differentiation and loss of cells, which can provide effective guidance and basis for the diagnosis of primary bladder tumors, which is an important factor for judging the pathological stage and prognosis of patients and can provide a theoretical reference for the formulation of therapeutic measures.
    Subjects
    Age; Alcohol; Biomedical research; Bladder; Bladder cancer; Cancer therapies; Cell differentiation; Cell Differentiation - genetics; Clonal deletion; Complications and side effects; Correlation analysis; Development and progression; Differentiation (biology); Disease; DNA, Viral; Gender; Health aspects; Human papillomavirus; Human papillomavirus 16 - genetics; Humans; Infections; Males; Malignancy; Medical prognosis; Papillomaviridae - genetics; Papillomavirus infections; Papillomavirus Infections - pathology; Pathology; Patients; Physiological aspects; Prognosis; Statistical analysis; Tumors; Urinary Bladder - pathology; Urinary Bladder Neoplasms - genetics; Urinary Bladder Neoplasms - pathology
  • Article

    Muscles within muscles: a tensiomyographic and histochemical analysis of the normal human vastus medialis longus and vastus medialis obliquus muscles

    Authors
    Travnik, Ludvik; Djordjevič, Srdjan; Rozman, Sergej; Hribernik, Marija; Dahmane, Raja
    Part of
    Journal of anatomy, 2013-06, Vol.222 (6), p.580-587
    Abstract
    • The aim of this study was to show the connection between structure (anatomical and histochemical) and function (muscle contraction properties) of vastus medialis obliquus (VMO) and vastus medialis longus (VML). The non-invasive tensiomyography (TMG) method was used to determine the contractile properties (contraction time; T(c)) of VML and VMO muscle, as a reflection of the ratio between the slow and fast fibers in two groups of nine young men. VML and VMO significantly (P < 0.01) differ in the proportion of type 1 (59.6: 44%) and type 2b (6.3: 15%) fibers. The VML muscle is almost entirely composed of type 1 and type 2a fibers. In many samples of this muscle no type 2b fibers were found. The proportion of slow-twitch type 1 fibers is nearly twice as high as the proportion of fast-twitch type 2a fibers. These observations indicate that VML is a slower and more fatigue-resistant muscle than VMO muscle. These characteristics correspond to the different functions of the VML, which is an extensor of the knee, and to the VMO, which maintains the stable position of the patella in the femoral groove. Our results obtained by TMG provided additional evidence that muscle fibers within the segments of VM muscle were not homogenous with regard to their contractile properties, thereby confirming the histochemical results. T(c) can be attributed to the higher percentage of slow-twitch fibers - type 1. The statistically shorter T(c) (P ≤ 0.001) of VMO (22.8 ± 4.0 ms) compared with VML (26.7 ± 4.0 ms) in our study is consistent with previously found differences in histochemical, morphological and electrophysiological data. In conclusion, the results of this study provide evidence that the VML and VMO muscles are not only anatomically and histochemically different muscles, but also functionally different biological structures.
    Subjects
    Adenosine Triphosphatases - metabolism; Adolescent; Adult; Autopsy; Electromyography - methods; Humans; Knee; Knee Joint - physiology; Male; Muscle Contraction - physiology; Muscle Fibers, Fast-Twitch - physiology; Muscle Fibers, Slow-Twitch - physiology; Muscular system; Original; Quadriceps Muscle - anatomy & histology; Quadriceps Muscle - physiology; Young Adult
  • Article

    Overexpressed long noncoding RNA TUG1 affects the cell cycle, proliferation, and apoptosis of pancreatic cancer partly through suppressing RND3 and MT2A

    Authors
    Hui, Bingqing; Xu, Yetao; Zhao, Benpeng; Ji, Hao; Ma, Zhonghua; Xu, Shufen; He, ZhenYu; Wang, Keming; Lu, Jianwei
    Part of
    OncoTargets and therapy, 2019-02, Vol.12, p.1043-1057
    Abstract
    • Long noncoding RNAs (lncRNAs) are involved in various human diseases, including cancers. However, their mechanisms remain undocumented. We investigated alterations in lncRNA that may be related to pancreatic cancer (PC) through analysis of microarray data. In the present study, quantitative real-time PCR analysis was used to examine the expression of taurine upregulated 1 ( ) in PC tissue samples and PC cell lines. In PC cell lines, MTT assays, colony formation assays, and flow cytometry were used to investigate the effects of on proliferation, cell cycle regulation, and apoptosis. Moreover, we established a xenograft model to assess the effect of on tumor growth in vivo. The molecular mechanism of potential target genes was detected through nuclear separation experiments, RNA immunoprecipitation (RIP), chromatin immunoprecipitation assays (ChIP), and other experimental methods. The findings suggest that the abnormally high expression of in PC tissues was associated with tumor size and pathological stage. Knockdown of blocked the cell cycle and accelerated apoptosis, thereby inhibiting the proliferation of PC cells. In addition, RIP experiments showed that can recruit enhancer of zeste homolog 2 (EZH2) to the promoter regions of Rho family GTPase 3 ( ) and metallothionein 2A ( ) and inhibit their expression at the transcriptional level. Furthermore, ChIP experiments demonstrated that EZH2 could bind to the promoter regions of and . The knockdown of reduced this binding capacity. In conclusion, our data suggest that may regulate the expression of PC-associated tumor suppressor genes at the transcriptional level and these may become potential targets for the diagnosis and treatment of PC.
    Subjects
    Antisense RNA; Apoptosis; Cell cycle; Chromatin; Development and progression; Genes; Genetic transcription; Long non-coding RNA; Original Research; Pancreatic cancer; Proliferation; RND3 and MT2A; Scientific equipment and supplies industry; TUG1
  • Article

    RETRACTED: Invasion of trophoblast cell lines is inhibited by miR-93 via MMP-2

    Authors
    Pan, Qiong; Niu, HuiYuan; Cheng, LongFei; Li, XiaoQiong; Zhang, QiGang; Ning, Ying
    Part of
    Placenta (Eastbourne), 2017-05, Vol.53, p.48-53
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editors. Western Blots from Figure 2A are similar to Western Blots from Figures 3A,D of Reference [1], Figures 3A,D of Reference [2], Figure 1A of Reference [3], Figures 2A,D of Reference [4], Figures 1A,B of Reference [5], Figures 2A,B of Reference [6], Figures 2A,B of Reference [7] and Figures 2A,B of Reference [8]. Panels of Figure 3A are similar to panels of Figure 2B of Reference [1], Figure 3A of Reference [8] and Figures 3E,F of Reference [9]. One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. Re-use of any data should be appropriately cited. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process. References[1]Yongfang Wang, Lianhong Xu, Lixin Jiang, Biochemical and Biophysical Research Communications (BBRC) 458 (2015) 714-719 http://dx.doi.org/10.1016/j.bbrc.2015.02.033.[2]Hong Zhu, Mei-hua Miao, Xue-qiang Ji, Jun Xue, Xue-jun Shao, BBRC 459 (2015) 340-345 http://dx.doi.org/10.1016/j.bbrc.2015.02.116.[3]Mingchen Shao, Yiwei Geng, Peng Lu, Ying Xi, Sidong Wei, Liuxing Wang, Qingxia Fan, Wang Ma, BBRC 464 (2015) 1309-1313 http://dx.doi.org/10.1016/j.bbrc.2015.07.128.[4]Xiangrui Meng, Peng Lu, Qingxia Fan, BBRC 470 (2016) 187-191 http://dx.doi.org/10.1016/j.bbrc.2016.01.025.[5]Junzhao Wu, Peng Yuan, Qixin Mao, Peng Lu, Tian Xie, Hanzhao Yang, Chengzheng Wang, BBRC 478 (2016) 274-278 http://dx.doi.org/10.1016/j.bbrc.2016.07.031.[6]Wenxian Cui, Yuanguo Li, Keqing Xu, Guijin Chen, Xiaoqun Lu, Qiuqin Duan, Zhirong Kang, BBRC 479 (2016) 901-906 http://dx.doi.org/10.1016/j.bbrc.2016.09.076.[7]Mingjun Bi, Wei Chen, Hongmei Yu, Jinxiu Wang, Fang Ding, Dong Jing Tang, Cuiyan Tang, BBRC 480 (2016) 369-374 http://dx.doi.org/10.1016/j.bbrc.2016.10.055.[8]Wenjun Tian, Guanghai Wang, Yiqing Liu, Zhenglan Huang, Caiqing Zhang, Kang Ning, Cuixiang Yu, Yajuan Shen, Minghui Wang, Yuantang Li, Yong Wang, Bingchang Zhang, Yaoran Zhao, BBRC 485 (2017) 35-40 http://dx.doi.org/10.1016/j.bbrc.2017.02.005.[9]Youcheng Xiu, Zan Liu, Shunyao Xia, Chengjun Jin, Huaifu Yin, Weiming Zhao, Qiong Wu, PLoS ONE 9(10) (2014) e109734 https://doi.org/10.1371/journal.pone.0109734.
  • Article

    RETRACTED: The miR-599 promotes non-small cell lung cancer cell invasion via SATB2

    Authors
    Tian, Wenjun; Wang, Guanghai; Liu, Yiqing; Huang, Zhenglan; Zhang, Caiqing; Ning, Kang; Yu, Cuixiang; Shen, Yajuan; Wang, Minghui; Li, Yuantang; Wang, Yong; Zhang, Bingchang; Zhao, Yaoran
    Part of
    Biochemical and biophysical research communications, 2017-03, Vol.485 (1), p.35-40
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. The Western blots from Figures 2A and 2B are similar to the Western blots from Figures 3A,D of Reference [1], Figures 3A,D of Reference [2], Figure 1A of Reference [3], Figures 2A,D of Reference [4], Figures 1A,B of Reference [5], Figures 2A,B of Reference [6] and Figures 2A,B of Reference [7]. Panels of Figure 3A are similar with panels of Figure 2B of Reference [1] and Figure 3E of Reference [8]. In addition, a significant amount of textual overlap has been noticed between this article and References [3] and [6]. One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. Re-use of any data should be appropriately cited. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process. References:[1]Yongfang Wang, Lianhong Xu, Lixin Jiang, Biochemical and Biophysical Research Communications (BBRC) 458 (2015) 714-719 http://dx.doi.org/10.1016/j.bbrc.2015.02.033.[2]Hong Zhu, Mei-hua Miao, Xue-qiang Ji, Jun Xue, Xue-jun Shao, BBRC 459 (2015) 340-345 http://dx.doi.org/10.1016/j.bbrc.2015.02.116.[3]Mingchen Shao, Yiwei Geng, Peng Lu, Ying Xi, Sidong Wei, Liuxing Wang, Qingxia Fan, Wang Ma, BBRC 464 (2015) 1309-1313 http://dx.doi.org/10.1016/j.bbrc.2015.07.128.[4]Xiangrui Meng, Peng Lu, Qingxia Fan, BBRC 470 (2016) 187-191 http://dx.doi.org/10.1016/j.bbrc.2016.01.025.[5]Junzhao Wu, Peng Yuan, Qixin Mao, Peng Lu, Tian Xie, Hanzhao Yang, Chengzheng Wang, BBRC 478 (2016) 274-278 http://dx.doi.org/10.1016/j.bbrc.2016.07.031.[6]Wenxian Cui, Yuanguo Li, Keqing Xu, Guijin Chen, Xiaoqun Lu, Qiuqin Duan, Zhirong Kang, BBRC 479 (2016) 901-906 http://dx.doi.org/10.1016/j.bbrc.2016.09.076.[7]Mingjun Bi, Wei Chen, Hongmei Yu, Jinxiu Wang, Fang Ding, Dong Jing Tang, Cuiyan Tang, BBRC 480 (2016) 369-374 http://dx.doi.org/10.1016/j.bbrc.2016.10.055.[8]Youcheng Xiu, Zan Liu, Shunyao Xia, Chengjun Jin, Huaifu Yin, Weiming Zhao, Qiong Wu, PLoS ONE 9(10) (2014) e109734 https://doi.org/10.1371/journal.pone.0109734.
  • Article

    Retracted: Cannabinoid CB(2) receptors modulate ERK‐1/2 kinase signalling and NO release in microglial cells stimulated with bacterial lipopolysaccharide, by S Merighi, S Gessi, K Varani, C Simioni, D Fazzi, P Mirandola and P A Borea. British Journal of Pharmacology, volume 165(6): 1773–1788, published in March 2012; DOI 10.1111/j.1476‐5381.2011.01673.x

    Part of
    British journal of pharmacology, 2017-08, Vol.174 (15), p.2609-2609
    Abstract
    • The above article, published by the British Journal of Pharmacology in March 2012 (http://onlinelibrary.wiley.com/doi/10.1111/j.1476‐5381.2011.01673.x/full), has been retracted by agreement between the authors, the Journal Editor in Chief and John Wiley & Sons Ltd. The authors wish to state that in preparation of the original manuscript errors occurred resulting in duplication. This issue relates specifically to Figures 2A and 2B, lanes 3‐5 of the pJNK1/2 in Figure 3B and lanes 1‐3 of the pJNK1/2 blot from Figure 3C. In addition, duplication has occurred in lanes 1‐9 of the total MEK1/2 blot (left) and lanes 1‐9 of the tubulin blot from Figure 6G JBC 280 (right). The authors apologize for the mistake. Unfortunately, the authors are not able to provide the original data for these figures.
    Subjects
    Bacteria; Extracellular signal-regulated kinase; Lipopolysaccharides; Microglial cells; Retraction; Tubulin
  • Article

    Cd induces G2/M cell cycle arrest by up-regulating miR-133b via directly targeting PPP2R2D in L02 hepatocytes

    Authors
    Zhang, Yujing; Xiao, Fang; Zhong, Caigao; Zeng, Ming; Zou, Lianhong
    Part of
    Metallomics, 2018-10, Vol.1 (1), p.151-1523
    Abstract
    • Previous research has shown that cadmium (Cd), which accumulates primarily in the liver and kidneys, could cause cell cycle arrest in various cell types. In the present study, the effect of Cd on the cell cycle progression of hepatocytes and the underlying mechanisms were investigated. Our results showed that Cd inhibited the growth and proliferation of L02 hepatocytes. Further study revealed that Cd significantly induced G2-phase cell cycle arrest accompanied by an overproduction of reactive oxygen species (ROS). Cd-induced G2-phase arrest could be prevented by inhibiting ROS with the use of antioxidant Trolox. Additionally, treatment with Cd induced an increase in the expression of miR-133b, which could be reversed with Trolox pretreatment. Moreover, miR-133b was shown to regulate PPP2R2D expression by binding to the 3′-untranslated region (UTR) of PPP2R2D mRNA. We also found that treatment with Cd decreased the expression of PPP2R2D , and inhibition of PPP2R2D expression by siRNA partially aggravated Cd-induced cell cycle arrest. By artificially increasing the expression of the protein phosphatase 2A-B55δ subunit (PP2A-B55δ, encoded by the PPP2R2D gene), we confirmed that PPP2R2D can be regulated by miR-133b in Cd-treated cells, and the G2-phase arrest effect could be suppressed by PP2A-B55δ. Collectively, these findings indicated that Cd increased ROS and induced the expression of miR-133b, which consequently inhibited the expression of PPP2R2D and led to G2-phase arrest in L02 hepatocytes. This study provides novel insights into the molecular mechanisms of Cd-induced cell cycle arrest. This study could provide a novel epigenetic mechanism for Cd-induced acute hepatotoxicity and it would offer new targets for its intervention.
    Subjects
    Antioxidants; Cadmium; Cell cycle; Eukaryotes; Gene expression; Hepatocytes; Inhibition; Kidneys; Liver; Molecular modelling; mRNA; Phosphoprotein phosphatase; Pretreatment; Protein phosphatase; Proteins; siRNA; Vitamin E
  • Article

    A tree of life based on ninety-eight expressed genes conserved across diverse eukaryotic species

    Authors
    Jayaswal, Pawan Kumar; Dogra, Vivek; Shanker, Asheesh; Sharma, Tilak Raj; Singh, Nagendra Kumar
    Part of
    PloS one, 2017-09, Vol.12 (9), p.e0184276-e0184276
    Abstract
    • Rapid advances in DNA sequencing technologies have resulted in the accumulation of large data sets in the public domain, facilitating comparative studies to provide novel insights into the evolution of life. Phylogenetic studies across the eukaryotic taxa have been reported but on the basis of a limited number of genes. Here we present a genome-wide analysis across different plant, fungal, protist, and animal species, with reference to the 36,002 expressed genes of the rice genome. Our analysis revealed 9831 genes unique to rice and 98 genes conserved across all 49 eukaryotic species analysed. The 98 genes conserved across diverse eukaryotes mostly exhibited binding and catalytic activities and shared common sequence motifs; and hence appeared to have a common origin. The 98 conserved genes belonged to 22 functional gene families including 26S protease, actin, ADP-ribosylation factor, ATP synthase, casein kinase, DEAD-box protein, DnaK, elongation factor 2, glyceraldehyde 3-phosphate, phosphatase 2A, ras-related protein, Ser/Thr protein phosphatase family protein, tubulin, ubiquitin and others. The consensus Bayesian eukaryotic tree of life developed in this study demonstrated widely separated clades of plants, fungi, and animals. Musa acuminata provided an evolutionary link between monocotyledons and dicotyledons, and Salpingoeca rosetta provided an evolutionary link between fungi and animals, which indicating that protozoan species are close relatives of fungi and animals. The divergence times for 1176 species pairs were estimated accurately by integrating fossil information with synonymous substitution rates in the comprehensive set of 98 genes. The present study provides valuable insight into the evolution of eukaryotes.
    Subjects
    Actin; Adenosine diphosphate; ADP-ribosylation factor; Analysis; Animal species; Animals; ATP synthase; Bayesian analysis; Biological evolution; Biology and Life Sciences; Biomedical materials; Biotechnology; Casein; Catalysis; Cereals; Comparative studies; Computer and Information Sciences; Deoxyribonucleic acid; Divergence; DNA; DNA sequencing; DnaK protein; Elongation; Eukaryotes; Evolution; Evolution, Molecular; Evolutionary genetics; Fungi; Fungi - genetics; Fungi - metabolism; Gene expression; Gene Expression Regulation, Fungal - physiology; Gene Expression Regulation, Plant - physiology; Gene families; Gene sequencing; Genes; Genes, Fungal - physiology; Genes, Plant - physiology; Genetic aspects; Genomes; Genomics; Glyceraldehyde; Glyceraldehyde 3-phosphate; Mammals; Pelodiscus sinensis; Phosphates; Phylogenetics; Phylogeny; Physiological aspects; Plants - genetics; Plants - metabolism; Protein phosphatase; Protozoa; Public domain; Research and Analysis Methods; Species; Surgical implants; Taxa; Tubulin; Ubiquitin
  • Article

    RETRACTED: miR-543 is up-regulated in gefitinib-resistant non-small cell lung cancer and promotes cell proliferation and invasion via phosphatase and tensin homolog

    Authors
    Bi, Mingjun; Chen, Wei; Yu, Hongmei; Wang, Jinxiu; Ding, Fang; Tang, Dong Jing; Tang, Cuiyan
    Part of
    Biochemical and biophysical research communications, 2016-11, Vol.480 (3), p.369-374
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. The Western blots from Figures 2A and 2B are similar to the Western blots from Figures 3A,D of Reference [1], Figures 3A,D of Reference [2], Figure 1A of Reference [3], Figures 2A,D of Reference [4], Figures 1A,B of Reference [5], Figures 2A,B of Reference [6]. In addition, a significant amount of textual overlap has been noticed between this article and References [4] and [6]. One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. Re-use of any data should be appropriately cited. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process. References:[1]Yongfang Wang, Lianhong Xu, Lixin Jiang, Biochemical and Biophysical Research Communications (BBRC) 458 (2015) 714-719 http://dx.doi.org/10.1016/j.bbrc.2015.02.033.[2]Hong Zhu, Mei-hua Miao, Xue-qiang Ji, Jun Xue, Xue-jun Shao, BBRC 459 (2015) 340-345 http://dx.doi.org/10.1016/j.bbrc.2015.02.116.[3]Mingchen Shao, Yiwei Geng, Peng Lu, Ying Xi, Sidong Wei, Liuxing Wang, Qingxia Fan, Wang Ma, BBRC 464 (2015) 1309-1313 http://dx.doi.org/10.1016/j.bbrc.2015.07.128.[4]Xiangrui Meng, Peng Lu, Qingxia Fan, BBRC 470 (2016) 187-191 http://dx.doi.org/10.1016/j.bbrc.2016.01.025.[5]Junzhao Wu, Peng Yuan, Qixin Mao, Peng Lu, Tian Xie, Hanzhao Yang, Chengzheng Wang, BBRC 478 (2016) 274-278 http://dx.doi.org/10.1016/j.bbrc.2016.07.031.[6]Wenxian Cui, Yuanguo Li, Keqing Xu, Guijin Chen, Xiaoqun Lu, Qiuqin Duan, Zhirong Kang, BBRC 479 (2016) 901-906 http://dx.doi.org/10.1016/j.bbrc.2016.09.076.
  • Article

    RETRACTED: Autophagy is a pro-survival mechanism in ovarian cancer against the apoptotic effects of euxanthone

    Authors
    Zhu, Li; Liu, Xiuping; Li, Dongmei; Sun, Shuhong; Wang, Yue; Sun, Xianghong
    Part of
    Biomedicine & pharmacotherapy, 2018-07, Vol.103, p.708-718
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief and the corresponding author as panels from Figure 2A appear as similar to panels from Figure 3A of the article published by Xiangyang Dou, Meihua Wang, Tao Zhang and Jiapei Yao in The Anatomical Record (2019) https://doi.org/10.1002/ar.24324 and Figure 2A of the article published by Qiang Wang, Yi Yan, Jie Zhang, Peng Guo, Yuqing Xing, Yong Wang, Fawei Qin and Qingyun Zeng in Biomedicine & Pharmacotherapy 104 (2018) 28-35 https://doi.org/10.1016/j.biopha.2018.05.013. Moreover, panels from Figure 2B appear as similar (after vertical mirroring) to panels from Figure 2A of the article published by Ning Wang, Fang Zhou, Jinhui Guo, Huaiyuan Zhu, Shanshui Luo and Jingjing Cao in Life Sciences 209 (2018) 498-506 https://doi.org/10.1016/j.lfs.2018.08.052. Also, panels from Figure 7C appear as similar to panels from Figure 8D of the article published by Zichao Li, Luying Zhang, Mingquan Gao, Mei Han, Kaili Liu, Zhuang Zhang, Zhi Gong, Lifei Xing, Xianzhou Shi, Kui Lu and Hui Gao in the Journal of Experimental & Clinical Cancer Research 38:8 (2019) https://doi.org/10.1186/s13046-018-1012-z. Although this article was published earlier than the other articles, the Editor decided to retract this article given the concerns on the reliability of the data. The corresponding author acknowledged that some of the TUNEL, Flow Cytometry and Immunohistochemistry (IHC) measurements have been provided by third party entities. One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. Re-use of any data should be appropriately cited. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process.
    Subjects
    Animals; Apoptosis - drug effects; Apoptosis - physiology; Autophagy - drug effects; Autophagy - physiology; Cell Line, Tumor; Cell Survival - drug effects; Cell Survival - physiology; Female; Humans; Male; Mice; Mice, Inbred BALB C; Mice, Nude; Ovarian Neoplasms - drug therapy; Ovarian Neoplasms - pathology; Random Allocation; Xanthones - therapeutic use; Xanthones - toxicity; Xenograft Model Antitumor Assays - methods
  • Article

    RETRACTED: circTulp4 functions in Alzheimer’s disease pathogenesis by regulating its parental gene, Tulp4

    Authors
    Ma, Nana; Pan, Jie; Wen, Yi; Wu, Qi; Yu, Bo; Chen, Xi; Wan, Jun; Zhang, Wei
    Part of
    Molecular therapy, 2021-06, Vol.29 (6), p.2167-2181
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. Concern has been raised by a reader that research reported in the article duplicates figures and reuses data from prior publications without attribution. After investigation of the concerns raised, the editors found the following reuse of data without attribution: Figure 1B in this article is identical to Ma et al., 2020, FASEB J. 34, 10342–10356, https://doi.org/10.1096/fj.201903157R, Figure 2B. Figure 1D in this article is identical to Ma et al., 2019, Mol. Ther. Nucleic Acids 18, 1049–1062, https://doi.org/10.1016/j.omtn.2019.10.030, Figure 2A. Figure 1F in this article is identical to Ma et al., 2019, Mol. Ther. Nucleic Acids 18, 1049–1062, https://doi.org/10.1016/j.omtn.2019.10.030, Figure 2B. Figure 1A in this article reuses data from Ma et al., 2020, FASEB J. 34, 10342–10356, https://doi.org/10.1096/fj.201903157R, Figure 2E. Figure S1 in this article is identical to Ma et al., 2019, Mol. Ther. Nucleic Acids 18, 1049–1062, https://doi.org/10.1016/j.omtn.2019.10.030, Figure 3 One of the conditions of submission of a paper for publication is that authors declare explicitly that the paper has not been previously published and is not under consideration for publication elsewhere. As such this article represents a misuse of the scientific publishing system. The corresponding authors have agreed to the retraction.
    Subjects
    Alzheimer Disease - etiology; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Animals; Biomarkers; Cell Differentiation - genetics; Disease Models, Animal; Disease Susceptibility; Gene Expression Profiling; Gene Expression Regulation; Gene Knockdown Techniques; Intracellular Signaling Peptides and Proteins - genetics; Mice; Mice, Transgenic; Models, Biological; Neuronal Outgrowth; Neurons - cytology; Neurons - metabolism; Nucleotide Motifs; RNA Polymerase II - metabolism; RNA Transport; RNA, Circular
  • Article

    Analysis of YAP1 and TAZ expression by immunohistochemical staining in malignant mesothelioma and reactive mesothelial cells

    Authors
    Takehara, Yusuke; Yamochi, Toshiko; Nagumo, Tasuku; Cho, Tomonari; Urushibara, Fumihiko; Ono, Kohei; Fujii, Tomonori; Okamoto, Naoko; Sasaki, Yosuke; Tazawa, Sakiko; Honma, Mayumi; Norose, Tomoko; Shiozawa, Eisuke; Tate, Genshu; Takimoto, Masafumi
    Part of
    Oncology letters, 2018-05, Vol.15 (5), p.6825-6830
    Abstract
    • Gene mutations are involved in the development of malignant mesothelioma. Important mutations have been identified in the genes for cyclin-dependent kinase inhibitor 2A (p16) alternative reading frame, breast cancer-associated protein 1 ( ) and neurofibromatosis type 2 ( ). Previously, the utility of detecting the loss of by immunohistochemistry (IHC) and p16-deletion by fluorescence hybridization has been identified in several studies. However, -associated examinations have not been performed. The present study aimed to evaluate the expression of yes-associated protein 1 (YAP1) and tafazzin (TAZ) protein, which are associated with gene mutations, in malignant mesothelioma (MM) and reactive mesothelial cells (RMCs). Formalin-fixed paraffin-embedded tissues from 31 MM and 33 RMC samples were analyzed. The expression of YAP1 and TAZ protein were examined by IHC. Positivity for YAP1 was identified 27/31 MM and 15/33 RMC samples. Positivity for TAZ was identified in 28/31 MM and 18/33 RMC samples. Using the optimal cutoff points determined by the receiver operating characteristic curve, a positive IHC result for YAP1 and TAZ was 74% sensitive and 94% specific for detecting MM. The results indicate that increased expression of YAP1 and TAZ may be associated with mesothelial tumorization, and aid in the diagnosis of MM.
    Subjects
    Age; Antigens; Care and treatment; Cell adhesion & migration; Cell division; Cell growth; Cytoplasm; Development and progression; Gene mutation; Gene mutations; Genetic aspects; Health aspects; Heat; Immunohistochemistry; Kinases; Laboratories; Medicine; Mesothelioma; Methods; Mutation; Patients; Proteins; Signal transduction; Signaling peptides and proteins; Studies; Thyroid gland; Transcription factors; Transferases
  • Article

    RETRACTED ARTICLE: A mechanistic model of the neural entropy increase elicited by psychedelic drugs

    Authors
    Herzog, Rubén; Mediano, Pedro A. M.; Rosas, Fernando E.; Carhart-Harris, Robin; Perl, Yonatan Sanz; Tagliazucchi, Enzo; Cofre, Rodrigo
    Part of
    Scientific reports, 2020-10, Vol.10 (1), Article 17725
    Abstract
    • Abstract Psychedelic drugs, including lysergic acid diethylamide and other agonists of the serotonin 2A receptor (5HT2A-R), induce drastic changes in subjective experience, and provide a unique opportunity to study the neurobiological basis of consciousness. One of the most notable neurophysiological signatures of psychedelics, increased entropy in spontaneous neural activity, is thought to be of relevance to the psychedelic experience, mediating both acute alterations in consciousness and long-term effects. However, no clear mechanistic explanation for this entropy increase has been put forward so far. We sought to do this here by building upon a recent whole-brain model of serotonergic neuromodulation, to study the entropic effects of 5HT2A-R activation. Our results reproduce the overall entropy increase observed in previous experiments in vivo, providing the first model-based explanation for this phenomenon. We also found that entropy changes were not uniform across the brain: entropy increased in some regions and decreased in others, suggesting a topographical reconfiguration mediated by 5HT2A-R activation. Interestingly, at the whole-brain level, this reconfiguration was not well explained by 5HT2A-R density, but related closely to the topological properties of the brain’s anatomical connectivity. These results help us understand the mechanisms underlying the psychedelic state and, more generally, the pharmacological modulation of whole-brain activity.
    Subjects
    Psychedelic drugs
  • Article

    RETRACTED: Down-regulated microRNA-195-5p and up-regulated CXCR4 attenuates the heart function injury of heart failure mice via inactivating JAK/STAT pathway

    Authors
    Shen, Yuhua; Zhang, Wen; Lee, Lijun; Hong, Mianming; Lee, Minfei; Chou, Guohui; Yu, Li; Sui, Yuqing; Chou, Baihua
    Part of
    International immunopharmacology, 2020-05, Vol.82, p.106225-106225, Article 106225
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. Concern was raised about the integrity of the images in Figure 6, which appear to contain suspected image duplications, as detailed here: https://pubpeer.com/publications/A31DE9EEF13ED6B88BCC86A9CAC8D9 and here: https://docs.google.com/spreadsheets/d/1r0MyIYpagBc58BRF9c3luWNlCX8VUvUuPyYYXzxWvgY/edit#gid=262337249. Most of these image duplications involve either pasting portions of one image into another, or rotating/flipping the image. Numerous additional suspected image duplications were detected within Figures 2A and 7A. The journal requested the corresponding author comment on these concerns and provide the raw data. The authors did not respond to this request and therefore the Editor-in-Chief decided to retract the article.
  • Article

    Efficacy and Safety of Peginterferon α-2a and Entecavir Tenofovir in the Treatment of Chronic Hepatitis B Genotype C

    Authors
    Yu, Jiao; Xu, Dong
    Part of
    Contrast media and molecular imaging, 2022-09, Vol.2022, p.7623832-8
    Abstract
    • This article discusses the clinical value of Pegylated Interferon (PEG-IFN) α-2a combined with entecavir or tenofovir in the treatment of Chronic Hepatitis B (CHB) genotype C patients. 78 patients with CHB genotype C were divided into three groups: control group, entecavir group, and tenofovir group according to different treatment methods. The efficacy and adverse reaction (AR) of the three groups are observed during 12 months of treatment and after drug withdrawal, and the clinical efficacy and safety of the three treatment methods are evaluated. The experimental results show that the sustained response rate (RR) in the tenofovir and entecavir groups is higher than that in the controls. The incidence of total AR in the tenofovir group is significantly higher than that in the control and entecavir groups. PEG-IFN α-2a and entecavir or tenofovir are more effective, and tenofovir has an antiviral effect.
    Subjects
    Antiviral Agents - therapeutic use; Genotype; Guanine - analogs & derivatives; Hepatitis B, Chronic - drug therapy; Humans; Interferon-alpha - adverse effects; Polyethylene Glycols - therapeutic use; Recombinant Proteins; Tenofovir - adverse effects; Treatment Outcome
  • Article

    RETRACTED: MiR-650 regulates the proliferation, migration and invasion of human oral cancer by targeting growth factor independent 1 (Gfi1)

    Authors
    Ningning, Sun; Libo, Sun; Chuanbin, Wu; Haijiang, Sun; Qing, Zhou
    Part of
    Biochimie, 2019-01, Vol.156, p.69-78
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. Following concerns raised by Dr. E. Bik and an anonymous reader, the journal conducted an investigation and found evidence that there had been improper manipulation and duplication of images in Figures 2A, 5C and 6C, as shown by partial overlap between images representing different experiments. An anonymous reader has also drawn attention to flow-cytometry data in Figure 1 similar to previously published data from a different laboratory (Med Sci Monit, 2018; 24: 5874-5880 DOI: 10.12659/MSM.909682, Figure 2B). After raising the complaint with the authors, the corresponding author agreed that the paper needed to be retracted. The authors apologise for any confusion that may have arisen from their article.
    Subjects
    Animals; Cell Line, Tumor; Cell Movement; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; G1 Phase Cell Cycle Checkpoints; Humans; Male; Mice; Mice, Inbred BALB C; Mice, Nude; MicroRNAs - genetics; MicroRNAs - metabolism; Mouth Neoplasms; Neoplasm Invasiveness; Neoplasm Proteins - genetics; Neoplasm Proteins - metabolism; RNA, Neoplasm - genetics; RNA, Neoplasm - metabolism; Transcription Factors - genetics; Transcription Factors - metabolism
  • Article

    RETRACTED: Possible involvement of the HMGB1/RAGE signaling mechanism in the induction of central post-stroke pain induced by acute global cerebral ischemia

    Authors
    Harada, Shinichi; Matsuura, Wataru; Liu, Keyue; Nishibori, Masahiro; Tokuyama, Shogo
    Part of
    Brain Research, 2016-09, Vol.1646, p.433-440
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Authors following an investigation into data manipulation (Figures 2A,B and 5) by an Investigation Committee at Kobe Gakuin University. Namely: Figures 2A and 2B - numerical disagreement (numbers removed) was found in some parts between the raw data and the article data, hence the significant difference illustrated in the published article was not obtained. Figure 5 - multiple numbers of the original raw data were changed, hence significant difference the significant difference illustrated in the published article was not obtained.
    Subjects
    Animals; Animals, Outbred Strains; Antibodies, Monoclonal - administration & dosage; Brain Ischemia - complications; Brain Ischemia - metabolism; Developmental Biology; Extracellular Signal-Regulated MAP Kinases - metabolism; General Neuroscience; HMGB1 Protein - immunology; HMGB1 Protein - metabolism; Hyperalgesia - metabolism; Injections, Intraventricular; Male; Mice; Molecular Biology; Neurology (clinical); Pain - etiology; Pain - metabolism; Phosphorylation; Receptor for Advanced Glycation End Products - metabolism; Sciatic Nerve - metabolism; Signal Transduction; Spinal Cord - metabolism; Stroke - complications; Stroke - metabolism
  • Article

    RETRACTED: Osthole decreases tau protein phosphorylation via PI3K/AKT/GSK-3β signaling pathway in Alzheimer's disease

    Authors
    Yao, Yingjia; Wang, Yameng; Kong, Liang; Chen, Yuqing; Yang, Jingxian
    Part of
    Life sciences (1973), 2019-01, Vol.217, p.16-24
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of Editor-in-Chief. The corresponding author notified the journal of image duplications within the published article and requested a corrigendum. Specifically, the ‘APP/PS1’ plot in Figure 1A had appeared in a previous publication [Panaxadiol inhibits synaptic dysfunction in Alzheimer's disease and targets the Fyn protein in APP/PS1 mice and APP-SH-SY5Y cells, Life Sciences (DOI: 10.1016/j.lfs.2019.03.070)], as the ‘TG’ plot in Figure 2A. In addition, several image duplications were identified within the panels of Figure 2. These issues, and others relating to unusual characteristics within the western blots, have been detailed here: https://pubpeer.com/publications/892AF7E4913255548C1446247FC65A#. As per journal policy when considering corrigendum requests, the journal requested the authors to provide explanations and source data relating to these affected figures. Upon receipt of additional source data, the editorial team noticed additional suspected image duplications. In relation to Figure 1A, the corresponding author stated that “…we mistakenly used the same Morris Water Maze data”, and a corrected figure was submitted. In relation to the image duplications within Figure 2, the corresponding author stated “…we mistakenly used the copy-and-paste tool instead of a color adjustment tool” during image post-processing. The corresponding author was unable to produce original unaltered and uncropped western blot source data. The editorial team have concerns about the provenance of the data and therefore the Editor-in-Chief decided to retract the article.
    Subjects
    Alzheimer Disease - drug therapy; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Alzheimer Disease - physiopathology; Animals; Apoptosis - drug effects; Coumarins - therapeutic use; Glycogen Synthase Kinase 3 beta - metabolism; Hippocampus - drug effects; Hippocampus - metabolism; Hippocampus - pathology; Hippocampus - physiopathology; Memory - drug effects; Mice, Inbred C57BL; Neuroprotective Agents - therapeutic use; Phosphatidylinositol 3-Kinases - metabolism; Phosphorylation - drug effects; Proto-Oncogene Proteins c-akt - metabolism; Signal Transduction - drug effects; tau Proteins - metabolism
  • Article

    RETRACTED: The interplay between reactive oxygen and nitrogen species contributes in the regulatory mechanism of the nitro-oxidative stress induced by cadmium in Arabidopsis

    Authors
    Liu, Shiliang; Yang, Rongjie; Tripathi, Durgesh Kumar; Li, Xi; He, Wei; Wu, Mengxi; Ali, Shafaqat; Ma, Mingdong; Cheng, Qingsu; Pan, Yuanzhi
    Part of
    Journal of hazardous materials, 2018-02, Vol.344, p.1007-1024
    Abstract
    • This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor, after consultation with the corresponding author Dr. Shiliang Liu due to image issues. The article reused several images from the author's paper published in Environmental Pollution 239 (2018) 53-68 (which has been retracted due to image issues): Figures 1c, 1d, 2a, 2b, 2c, 4a, 9a and 9b. The article also plagiarized part of a paper from other authors that had appeared in Plant Physiology, 150, 229-243 (2009). The images that were reused were Fig 5 a, 5c, 5e and 5g. This was brought to the editors’ attention via a letter to the editor. One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. Re-use of any data should be appropriately cited. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of the journal that this was not detected during the submission process.
    Subjects
    Antioxidants - metabolism; Arabidopsis - drug effects; Arabidopsis - embryology; Arabidopsis - metabolism; Arabidopsis Proteins - metabolism; Cadmium - toxicity; Fluorescent Dyes - chemistry; Glutathione Reductase - metabolism; Nitric Oxide - biosynthesis; Oxidative Stress - drug effects; Reactive Nitrogen Species - metabolism; Reactive Oxygen Species - metabolism; S-Nitrosoglutathione - metabolism; Spectrophotometry, Atomic; Stress, Physiological - drug effects

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