PReD-Bench/PRed-Bench huggingface dataset:
Enhanced cancer therapy with the combination of EGFR and VEGFR-2 targeting in an orthotopic glioblastoma model
Authors: Yan-Lin Huang
Xin-Hua Tian
Lu-Kui Chen
Xiao-Ning Lin
Zai-Wang Zhuang
Yi Diao
Journal: Journal of Chemotherapy (2010)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: orthotopic glioblastoma model; monoclonal antibody; DC101; vascular endothelial growth factor receptor-2 (VEGFR-2); C225
Affiliations: Neurosurgical Department of Affiliated Zhongshan Hospital, Xiamen University, People's Republic of China.

Abstract:  Using an orthotopic glioblastoma model, we investigated the activity of the combination of monoclonal antibody DC101 against vascular endothelial growth factor receptor-2 (VEGFR-2) and monoclonal antibody C225 against epidermal growth factor receptor (EGFR). Nude mice bearing intracerebral glioblastoma xenografts were administered either DC101 or C225, or the combination via intraperitoneal (i.p.) injection. Histopathological analysis of solid tumor volume, microvessel density, tumor cell proliferation and apoptosis were performed. In the DC101-treated group, solid tumor volume and microvessel density were reduced by 59.7% and 64%, respectively. The tumor cell proliferation level was reduced by 53.2% and tumor cell apoptosis was increased by 66.7% but there was enhanced tumor cell invasiveness. C225 alone reduced the invasiveness of tumor tissue, but had no effect on solid tumor growth, microvessel density, tumor cell proliferation or apoptosis. The combination cancer therapy with C225 and DC101 enhanced tumor treatment with reduced tumor volume, microvessel density, tumor cell proliferation level, and increased cancer cell apoptosis, while decreasing tumor cell invasiveness. 

Retracted: No

PubPeer comments:
 Figure 4. * Pink boxes: Panels f (C225-treated tumors) and h (C225 combined with DC101-treated tumors) appear to show an overlap. ![file] , 
 Figure 5. At least three of the four panels shown appear to show the same specimen. * Blue boxes: The control and C225 panels appear to show an overlap. * Red boxes: The C225 and DC101 Panels appear to show an overlap. ![file] , 
 Figure 6. * Green boxes: the control and C225 panels appear to show an overlap, if one of the two panels is mirrored verrtically * Purple boxes: the DC101 and C225+DC101 panels appear to show an overlap ![file] , 
 Figure 5. * These four panels appear to be the same as those in Figure 6a of another paper by the same research group, i.e. Diao Yi et al., Journal of Neuro-Oncology (2011), doi: 10.1007 s11060-010-0479-z, https: pubpeer.com publications 158122B421877E48CD8EE3F8A1D915 ![file] , 
 Figure 6. * Purple boxes: The DC101 and C225+DC101 panels appear to overlap with panels in Figure 7 of the same 2011 paper as mentioned in comment #4, i.e. Diao Yi et al., Journal of Neuro-Oncology (2011), doi: 10.1007 s11060-010-0479-z, https: pubpeer.com publications 158122B421877E48CD8EE3F8A1D915 ![file] ,
The effect of transforming growth factor β1 on the crosstalk between autophagy and apoptosis in the annulus fibrosus cells under serum deprivation
Authors: Sheng-Dan Jiang
Yue-Hua Yang
Lei-Sheng Jiang
Bo Li
Jiang-Wei Chen
Ke Chen
Bin-Bin Ni
Journal: Cytokine (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Apoptosis; Autophagy; Disc degeneration; Serum deprivation; TGF-β1.
Affiliations: Department of Orthopedic Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China., Department of Orthopedic Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China. Electronic address: .

Abstract:  Autophagy and apoptosis are important in maintaining the metabolic homeostasis of intervertebral disc cells, and transforming growth factor-β1 (TGF-β1) is able to delay intervertebral disc degeneration. This study determined the effect of TGF-β1 on the crosstalk between autophagy and apoptosis in the disc cells, with the aim to provide molecular mechanism support for the prevention and treatment of disc degeneration. Annulus fibrosus (AF) cells were isolated and cultured under serum starvation. 10 ng/mL TGF-β1 reduced the apoptosis incidence in the cells under serum starvation for 48 h, down-regulated the autophagy incidence in the cells pretreated with 3-methyladenine (3-MA) or Bafilomycin A (Baf A), partly rescued the increased apoptosis incidence in the cells pretreated with 3-MA, while further reduced the decreased apoptosis incidence in the cells pretreated with Baf A. Meanwhile, TGF-β1 down-regulated the expressions of autophagic and apoptotic markers in the cells under starvation, partly down-regulated the expressions of Beclin-1, LC3 II/I and cleaved caspase-3 in the cells pretreated with 3-MA or Baf A, while significantly decreased the expression of Bax/Bcl-2 in the cells pretreated with Baf A. 3-MA blocked the phosphorylation of both AKT and mTOR and partly reduced the inhibitory effect of TGF-β1 on the expression of LC3 II/I and cleaved caspase-3. TGF-β1 enhanced the expression of p-ERK1/2 and down-regulated the expressions of LC3 II/I and cleaved caspase-3. U0126 partly reversed this inhibitory effect of TGF-β1. In conclusion, TGF-β1 protected against apoptosis of AF cells under starvation through down-regulating excessive autophagy. PI3K-AKT-mTOR and MAPK-ERK1/2 were the possible signaling pathways involved in this process. 

Retracted: No

PubPeer comments:
 Figure 3B. * Red boxes: Two panels appear to show very similar measurements, although they have been gated differently. Reported to the journal in October 2015 with several reminders, but no action as of now. ![file] ,
Overexpression of a Monocot Acyl‐CoA‐Binding Protein Confers Broad‐Spectrum Pathogen Protection in a Dicot
Authors: Mee-Len Chye
Pan Liao
Clive Lo
Paul W J Taylor
Saritha Panthapulakkal Narayanan
Journal: PROTEOMICS (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Alternaria brassicicola; Botrytis cinerea; Colletotrichum siamense; Pseudomonas syringae; Rhizoctonia solani
Affiliations: School of Biological SciencesThe University of Hong Kong Pokfulam Road Hong Kong China, Faculty of Veterinary and Agricultural SciencesUniversity of Melbourne Melbourne VIC 3010 Australia

Abstract:  Plants are continuously infected by various pathogens throughout their lifecycle. Previous studies have reported that the expression of Class III acyl-CoA-binding proteins (ACBPs) such as the Arabidopsis ACBP3 and rice ACBP5 were induced by pathogen infection. Transgenic Arabidopsis AtACBP3-overexpressors (AtACBP3-OEs) displayed enhanced protection against the bacterial biotroph, Pseudomonas syringae, although they became susceptible to the fungal necrotroph Botrytis cinerea. A Class III ACBP from a monocot, rice (Oryza sativa) OsACBP5 was overexpressed in the dicot Arabidopsis. The resultant transgenic Arabidopsis lines conferred resistance not only to the bacterial biotroph P. syringae but to fungal necrotrophs (Rhizoctonia solani, B. cinerea, Alternaria brassicicola) and a hemibiotroph (Colletotrichum siamense). Changes in protein expression in R. solani-infected Arabidopsis OsACBP5-overexpressors (OsACBP5-OEs) were demonstrated using proteomic analysis. Biotic stress-related proteins including cell wall-related proteins such as FASCILIN-LIKE ARABINOGALACTAN-PROTEIN10, LEUCINE-RICH REPEAT EXTENSIN-LIKE PROTEINS, XYLOGLUCAN ENDOTRANSGLUCOSYLASE/HYDROLASE PROTEIN4, and PECTINESTERASE INHIBITOR18; proteins associated with glucosinolate degradation including GDSL-LIKE LIPASE23, EPITHIOSPECIFIER MODIFIER1, MYROSINASE1, MYROSINASE2, and NITRILASE1; as well as a protein involved in jasmonate biosynthesis, ALLENE OXIDE CYCLASE2, were induced in OsACBP5-OEs upon R. solani infection. These results indicated that upregulation of these proteins in OsACBP5-OEs conferred protection against various plant pathogens. 

Retracted: No

PubPeer comments:
 Figure 1A has two panels that were duplicated. ![file] , 
 In Figure 2, some panels are duplicated (shown in red), and two other panels (in blue) are presenting the same plant, with the leaves slightly rearranged. ![file] ,
A Novel Role for FAK as a Protease-Targeting Adaptor Protein
Authors: Michael D Schaller
M Andrew Westhoff
Margaret C Frame
Neil O Carragher
Valerie J Fincham
Journal: Current Biology (2003)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cell migration; integrin-dependent adhesions; nonreceptor tyrosine kinases; Src; FAK

Abstract:  Cell migration on extracellular matrix requires the turnover of integrin-dependent adhesions. The nonreceptor tyrosine kinases Src and FAK regulate focal-adhesion turnover by poorly understood mechanisms. ERK/MAP kinase-mediated activation of the protease Calpain 2 also promotes focal-adhesion turnover; however, it is not known if this is linked to the activities of Src and FAK. Calpain 2 has previously been demonstrated to colocalize with focal-adhesion structures and can cleave several focal-adhesion complex components, including FAK. Studies utilizing Calpain inhibitors or Calpain-deficient cells confirm that Calpain's role in regulating focal-adhesion turnover is necessary for cell migration. We have identified a novel and kinase-independent function for FAK as an adaptor molecule that mediates the assembly of a complex consisting of at least Calpain 2 and p42ERK. Mutation of proline residues (Pro2) in the amino-terminal region of FAK blocks direct binding with Calpain 2 and also prevents formation of the Calpain 2/p42ERK complex in cells. We show that both complex formation and MEK/ERK activity are associated with Calpain-mediated proteolysis of FAK and focal adhesion turnover during transformation and migration. Furthermore, FAK is necessary for recruiting both Calpain 2 and p42ERK/MAPK to peripheral adhesion sites facilitating maximal Calpain activity. 

Retracted: No

PubPeer comments:
 Figure 1B. Vertical, straight changes in signal in Lysates c-myc FAK panel, but not in Lysates phosho-p42ERK panel. ![file] , 
 Figure 2B. Splices in phospho-p42ERK and FAK panels not accompanied by splices in the other panel. ![file] , 
 ![file] , 
 #3 Fig 1B. Many thanks for confirming that the the myc-FAK blot and phospho-p42ERK blot are from different experiments. Also, many thanks for confirming that the myc-FAK blot is spliced ( we removed the other myc-FAK-mutant lanes from the blot ). ,
RETRACTED CHAPTER: Technical Features and Challenges of the Paper-Based Colorimetric Assay
Authors: Kim, Insu
Lee, Dongtak
Yoon, Dae Sung
Lee, Sang Won
Lee, Gyudo
Journal: Bioanalysis (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Sensing devices; Diagnostic devices; Developing countries; World Health Organization; ASSURED

Abstract: The future of sensing and diagnostic devices for developing countries should be, as described by the World Health Organization (WHO), ASSURED: Affordable, Sensitive, Specific, User-friendly, Rapid and robust, Equipment free, and Deliverable to end users [1]....

Retracted: Yes

PubPeer comments:
 This book chapter (2021) plagiarized almost in its entirety this review paper from 2017: Technical aspects and challenges of colorimetric detection with microfluidic paper-based analytical devices (u03bcPADs) - A review . ,
FAM46B Promotes Apoptosis and Inhibits Glycolysis of Prostate Cancer Through Inhibition of the MYC-LDHA Axis
Authors: Xuxiao Ye
Chao Deng
Zuowei Li
Tao Liang
Binqiang Tian
Dongliang Yan
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: FAM46B; LDHA; glycolysis; prostate cancer.
Affiliations: Department of Urology, Shanghai Sixth People's Hospital East Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai 201306, People's Republic of China.

Abstract:  Objective: Increased dependence on glycolysis is a known element of cancer. This study was designed to examine critical glycolysis components including transcription factor MYC and its downstream target lactate dehydrogenase A (LDHA), potential upstream regulators of glycolysis such as family with sequence similarity 46 member B (FAM46B), and the impact of the abundance of these proteins on apoptosis and glycolysis in prostate cancer. Materials and methods: A total of 70 primary prostate cancer patient samples were compared to normal tissues for FAM46B and LDHA expression and the corresponding patients' survival was monitored for 60 months. Prostate cancer cell lines were employed for protein expression manipulation, glucose uptake and LDH assays, and apoptosis measurements. A xenograft mouse model was used to quantify the role of FAM46B and LDHA on tumor growth in vivo. Results: FAM46B expression was reduced in prostate tumor tissue compared to normal tissue and prostate cancer patients who expressed low amounts of FAM46B had shortened average lifespans compared to those who expressed higher amounts of FAM46B (p=0.008). FAM46B overexpression reduced glucose uptake, decreased LDH activity, and induced apoptosis in prostate cancer cell lines while FAM46B shRNA increased MYC levels in a non-malignant prostate cell line (P69). Conversely, forced expression of LDHA in LNCaP cells produced an increase in glycolysis markers with a corresponding decrease in apoptosis. FAM46B-overexpressing xenografts had starkly blunted growth which was restored with co-overexpression of LDHA. Conclusion: FAM46B plays a central role in regulating glycolysis and apoptosis in prostate cancer and operates through the regulation of LDHA via MYC. FAM46B's keystone status in prostate cancer makes it a potential, robust biomarker for prostate cancer prognosis and a promising therapeutic target. 

Retracted: No

PubPeer comments:
 Figure 3B: Two of the flow cytometry dot plots share similar patterns. Please compare shNC and shFAM46B-1. ![file] ,
TAp63gamma can substitute for p53 in inducing expression of the maspin tumor suppressor
Authors: Joachim Mössner
Kurt Engeland
Andrea Tannapfel
Katja Spiesbach
Journal: International Journal of Cancer (2005)
Discipline: CLINICAL MEDICINE
Keywords: Maspin; Tumor suppressor; p53; p63; TAp63gamma
Affiliations: Department of Internal Medicine II, University of Leipzig, Leipzig, Germany.

Abstract:  Maspin is a Class II tumor suppressor protein and plays a role in tumor growth by inhibiting cellular invasion and motility. It is a member of the serpin family of protease inhibitors and has been shown to reduce angiogenesis. Maspin gene expression can be upregulated by the tumor suppressor p53. We tested 7 p53-related proteins of the p63 and p73 families for their ability to induce maspin expression. The p63 splice form TAp63gamma can substitute for p53 in activating the maspin promoter. TAp63gamma activates the promoter through the same consensus site as p53. In the DLD-1 colorectal adenocarcinoma cell line, harboring a tet-off regulated transgene, induction of TAp63gamma leads to an upregulation of maspin mRNA from the chromosomal gene. With a short lag phase also maspin protein levels are elevated after induced TAp63gamma expression. To assess a potential function of p63-dependent maspin upregulation in tumors we followed expression of p53, p63 and maspin by immunohistochemistry in hepatocellular carcinomas. Two types of tumors with wild-type or mutant p53 were assayed. Interestingly, the majority of tumors expressing only a mutated and inactive p53 protein nonetheless stain positive for maspin, whereas these tumors were positive for p63 protein expression. In summary, we show that TAp63gamma can substitute for p53 in transcriptional activation of the maspin tumor suppressor gene. TAp63gamma employs the same DNA recognition site for this activation as p53. We observe expression patterns of p53, p63 and maspin proteins in tumor tissue that may indicate also a function of maspin induction by p63 in tumors. 

Retracted: No

PubPeer comments:
 ![file] , 
 2020 correction. https: onlinelibrary.wiley.com doi 10.1002 ijc.32811 The authors accidently presented identical bands for the u03b2u2010actin loading control in the left and right panel although the experimental setup of these panels was different. Because considerable time has passed since the paper was published, the original electronic scan of the Western Blot could not be located. However, a scan of the paper printout was retrieved and has now been used to compose the figure. In the revised figure, the bands for u03b2u2010actin are correctly shown and this change does not affect the outcome of the study. The authors apologize for these circumstances, which required clarification of the data. The correct version of Figure 1 is as follows: The authors apologize for any confusion. ,
Long non-coding RNA H19 contributes to hypoxia-induced CPC injury by suppressing Sirt1 through miR-200a-3p
Authors: Linlin Li
Haiqing Li
Zuyun Liu
Anqing Chen
Zhize Yuan
Qiuyun Wang
Zhe Wang
Journal: Acta biochimica et biophysica Sinica (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Cardiomyocyte death; myocardial infarction; heart failure; cardiac progenitor cells; myocardial regeneration
Affiliations: College of Life Sciences, Peking University, Beijing, China., Department of Cardiac Surgery, Ruijin Hospital, Shanghai, China.

Abstract:  Cardiomyocyte death is the chief obstacle that prevents the heart function recovery in myocardial infarction (MI)-induced heart failure (HF). Cardiac progenitor cells (CPCs)-based myocardial regeneration has provided a promising method for heart function recovery after MI. However, CPCs can easily lose their proliferation ability due to oxygen deficiency in infarcted myocardium. Revealing the underlying molecular mechanism for CPC proliferation is critical for effective MI therapy. In the present study, we set up a CoCl2-induced hypoxia model in CPCs. We found that the expression of long non-coding RNA H19 was significantly down-regulated in CPCs after hypoxia stimuli. In addition, H19 suppression attenuated the proliferation and migration of CPCs under hypoxia stress. Furthermore, we discovered that H19 regulated the proliferation and migration of CPCs through mediating the expression of Sirt1 which is a target of miR-200a-3p under hypoxia. In conclusion, our findings demonstrate a novel regulatory mechanism for the proliferation and migration of CPCs under hypoxia condition, which provides useful information for the development of new therapeutic targets for MI therapy. 

Retracted: No

PubPeer comments:
 Column 1 and Column 3 show the same EdU image acquisitions, although DAPI (nuclei stainings) differ. Could the authors check? ![file] ,
Metformin-associated lactic acidosis in an intensive care unit
Authors: Nicolas Peters
Nicolas Jay
Damien Barraud
Aurélie Cravoisy
Lionel Nace
Sébastien Gibot
Pierre-Edouard Bollaert
Journal: Critical Care (2008)
Discipline: CLINICAL MEDICINE
Keywords: Metformin-associated lactic acidosis; dialysis; mortality rate; ICU; prevalence
Affiliations: Service de Néphrologie, CHU Brabois; Vandoeuvre les Nancy, 54500, France. 

Abstract:  Introduction: Metformin-associated lactic acidosis (MALA) is a classic side effect of metformin and is known to be a severe disease with a high mortality rate. The treatment of MALA with dialysis is controversial and is the subject of many case reports in the literature. We aimed to assess the prevalence of MALA in a 16-bed, university-affiliated, intensive care unit (ICU), and the effect of dialysis on patient outcome. Methods: Over a five-year period, we retrospectively identified all patients who were either admitted to the ICU with metformin as a usual medication, or who attempted suicide by metformin ingestion. Within this population, we selected patients presenting with lactic acidosis, thus defining MALA, and described their clinical and biological features. Results: MALA accounted for 0.84% of all admissions during the study period (30 MALA admissions over five years) and was associated with a 30% mortality rate. The only factors associated with a fatal outcome were the reason for admission in the ICU and the initial prothrombin time. Although patients who went on to haemodialysis had higher illness severity scores, as compared with those who were not dialysed, the mortality rates were similar between the two groups (31.3% versus 28.6%). Conclusions: MALA can be encountered in the ICU several times a year and still remains a life-threatening condition. Treatment is restricted mostly to supportive measures, although haemodialysis may possess a protective effect. 

Retracted: No

PubPeer comments:
 The introduction of this paper contains several errors.  Metformin is a small molecule (165 kDa) with a 50% oral bio-availability The molecule studied, metformin, does NOT have a molecular weight of 165kDa. But rather 165 Da. A molecule with a MW of 165 kDa would not be considered small. ,
Protease-activated receptor 4 deficiency offers cardioprotection after acute ischemia reperfusion injury
Authors: Mikhail A Kolpakov
Satya P Kunapuli
Sahar Iftikhar
Bahman Hooshdaran
Joseph R Libonati
Abdelkarim Sabri
Yulia V Bashkirova
Khadija Rafiq
Liudmila Vlasenko
Tao Wang
Xiongwen Chen
Xiaoxiao Zhang
Xinji Guo
Journal: Journal of Molecular and Cellular Cardiology (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Apoptosis; Cardioprotection; Inflammation; Myocardial ischemia reperfusion; Thrombin receptor.
Affiliations: Cardiovascular Research Center and Department of Physiology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, USA., Department of Medicine, Center of Translational Medicine, Thomas Jefferson University, Philadelphia, PA, USA., Cardiovascular Research Center and Department of Physiology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, USA; Institute of Molecular and Cellular Biology, Siberian Branch of Russian Academy of Sciences, Novosibirsk, Russia., School of Nursing, University of Pennsylvania, Philadelphia, PA, USA., Cardiovascular Research Center and Department of Physiology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, USA. Electronic address: .

Abstract:  Protease-activated receptor (PAR)4 is a low affinity thrombin receptor with less understood function relative to PAR1. PAR4 is involved in platelet activation and hemostasis, but its specific actions on myocyte growth and cardiac function remain unknown. This study examined the role of PAR4 deficiency on cardioprotection after myocardial ischemia-reperfusion (IR) injury in mice. When challenged by in vivo or ex vivo IR, PAR4 knockout (KO) mice exhibited increased tolerance to injury, which was manifest as reduced infarct size and a more robust functional recovery compared to wild-type mice. PAR4 KO mice also showed reduced cardiomyocyte apoptosis and putative signaling shifts in survival pathways in response to IR. Inhibition of PAR4 expression in isolated cardiomyocytes by shRNA offered protection against thrombin and PAR4-agonist peptide-induced apoptosis, while overexpression of wild-type PAR4 significantly enhanced the susceptibility of cardiomyocytes to apoptosis, even under low thrombin concentrations. Further studies implicate Src- and epidermal growth factor receptor-dependent activation of JNK on the proapoptotic effect of PAR4 in cardiomyocytes. These findings reveal a pivotal role for PAR4 as a regulator of cardiomyocyte survival and point to PAR4 inhibition as a therapeutic target offering cardioprotection after acute IR injury. 

Retracted: No

PubPeer comments:
 Figure 1c Unusual repetition of noise in XRD pattern ![file] , 
 Figure 1 d Similar repetition of noise in XRD pattern ![file] , 
 Figure 2 h) EDS spectra. Again repetition of noise ![file] , 
 Figure 5 a Again EDS spectra ![file] ,
MicroRNA-139-5p modulates the growth and metastasis of malignant melanoma cells via the PI3K/AKT signaling pathway by binding to IGF1R
Authors: Jianying Liang
Yanchang Li
Lifei Zhu
Chaoying Yang
Zhaoxia Xia
Zhixin Zheng
Liangcai Wu
Journal: Cell Cycle (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: IGF1R; MicroRNA-139-5p; PI3K/AKT signaling pathway.
Affiliations: Department of Dermatology, The Sixth Affiliated Hospital of Sun Yat-senUniversity, Guangzhou, PR. China., Department of Ophthalmology, The Sixth Affiliated Hospital of Sun Yat-senUniversity, PR. China., Department of Dermatology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR.China.

Abstract:  The relation between microRNAs (miRNAs) and malignant melanoma has been demonstrated in previous studies, while there was little research about miR-139-5p and malignant melanoma. The aim of this study is to investigate the ability of miR-139-5p in malignant melanoma cells via the modulation of the PI3K/AKT signaling pathway by targeting IGF1R. MiR-139-5p expression in malignant melanoma tissues and 5 malignant melanoma cell lines was detected. The melanoma cells were transfected with miR-139-5p mimic negative control (NC) sequence, miR-139-5p mimic, IGF1R overexpressed recombinant plasmid NC or IGF1R overexpressed sequence. The expression of Akt signaling pathway-related protein was evaluated. The biological functions in malignant melanoma cells were evaluated by a string of experiments. MiR-139-5p expressed a poor level in tissues and cell lines of malignant melanoma. Overexpressed miR-139-5p suppressed the cell proliferation, migration, and invasion, and contributed to the promoted apoptosis of malignant melanoma cells by decreasing IGF1R. MiR-139-5p down-regulated the IGF1R expression, and IGF1R accelerated the activation of the PI3K/AKT signaling pathway. miR-139-5p reversed the promotive impacts of IGF1R on the PI3K/AKT signaling pathway. The study validates that miR-139-5p could suppress malignant melanoma progression through the repression of the PI3K/AKT signaling pathway by down-regulating IGF1R. Therefore, miR-139-5p could pave a new way for the treatment of malignant melanoma. 

Retracted: No

PubPeer comments:
 Figure 2h, 2i and 4f have serious problems. ![file] , 
 Correction, [23 June 2020] .  It has been noted by the authors that the Figures 2 and 4 were published with errors. These errors have now been corrected as shown below. This correction has not changed the description, interpretation, or the original conclusions of the article. The authors apologize for any inconvenience caused. ![file] ![file]  Errors is an odd word for describing the features highlighted by Indigofera Tanganyikensis in Comment #1. Did they happen by accident? ,
Long Noncoding RNA ADINR Regulates Adipogenesis by Transcriptionally Activating C/EBPα
Authors: Robert Chunhua Zhao
Lihui Liu
Stephen Dalton
Tengfei Xiao
Shihua Wang
Tangping Li
Runsheng Chen
Huaxia Luo
Yu Sun
Hongling Li
Journal: Stem cell reports (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: C/EBPα; transcriptional regulator; adipogenesis; lncRNA; ADINR
Affiliations: Key Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; Key Laboratory of Non-coding RNA, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Harvard School of Public Health, Boston, MA 02215, USA., Key Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; Key Laboratory of Non-coding RNA, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; Graduate School of the Chinese Academy of Sciences, Beijing 100080, China., Center of Excellence in Tissue Engineering, Institute of Basic Medical Sciences, School of Basic Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China., Paul D. Coverdell Center for Biomedical and Health Sciences, Department of Biochemistry and Molecular Biology, The University of Georgia, 500 D.W. Brooks Drive, Athens, GA 30602, USA., Center of Excellence in Tissue Engineering, Institute of Basic Medical Sciences, School of Basic Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China. Electronic address: ., Key Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China; Key Laboratory of Non-coding RNA, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China. Electronic address: .

Abstract:  C/EBPα is a critical transcriptional regulator of adipogenesis. How C/EBPα transcription is itself regulated is poorly understood, however, and remains a key question that needs to be addressed for a complete understanding of adipogenic development. Here, we identify a lncRNA, ADINR (adipogenic differentiation induced noncoding RNA), transcribed from a position ∼450 bp upstream of the C/EBPα gene, that orchestrates C/EBPα transcription in vivo. Depletion of ADINR leads to a severe adipogenic defect that is rescued by overexpression of C/EBPα. Moreover, we reveal that ADINR RNA specifically binds to PA1 and recruits MLL3/4 histone methyl-transferase complexes so as to increase H3K4me3 and decrease H3K27me3 histone modification in the C/EBPα locus during adipogenesis. These results show that ADINR plays important roles in regulating the differentiation of human mesenchymal stem cells into adipocytes by modulating C/EBPα in cis. 

Retracted: No

PubPeer comments:
 Figures 2D and 2K appear to have a repeated image. *** ![file] , 
 Fig 3B,C. ![file] , 
 Enhanced-contrast version to focus on the background: ![file] , 
 #1 Three repeated images. ![] ,
Gnotobiotic rainbow trout (Oncorhynchus mykiss) model reveals endogenous bacteria that protect against Flavobacterium columnare infection
Authors: Jean-Marc Ghigo
Sol Vendrell-Fernández
Vincent Petit
Dimitri Rigaudeau
Rafael Patiño-Navarrete
Joaquín Bernal-Bayard
David Pérez-Pascual
Bianca Audrain
Journal: PLoS pathogens (2021)
Discipline: MICROBIOLOGY
Keywords: antibiotic use; aquaculture; bacterial probiotics; fish infections; larval stage
Affiliations: Unité de Génétique des Biofilms, Institut Pasteur, UMR CNRS2001, Paris, France., Ecologie et Evolution de la Résistance aux Antibiotiques, Institut Pasteur-APHP University Paris Sud, Paris, France., AQUALANDE, Gué de Bern, Pissos, France., Unité Infectiologie Expérimentale Rongeurs et Poissons, INRAE, Université Paris-Saclay, Jouy-en-Josas, France.

Abstract:  The health and environmental risks associated with antibiotic use in aquaculture have promoted bacterial probiotics as an alternative approach to control fish infections in vulnerable larval and juvenile stages. However, evidence-based identification of probiotics is often hindered by the complexity of bacteria-host interactions and host variability in microbiologically uncontrolled conditions. While these difficulties can be partially resolved using gnotobiotic models harboring no or reduced microbiota, most host-microbe interaction studies are carried out in animal models with little relevance for fish farming. Here we studied host-microbiota-pathogen interactions in a germ-free and gnotobiotic model of rainbow trout (Oncorhynchus mykiss), one of the most widely cultured salmonids. We demonstrated that germ-free larvae raised in sterile conditions displayed no significant difference in growth after 35 days compared to conventionally-raised larvae, but were extremely sensitive to infection by Flavobacterium columnare, a common freshwater fish pathogen causing major economic losses worldwide. Furthermore, re-conventionalization with 11 culturable species from the conventional trout microbiota conferred resistance to F. columnare infection. Using mono-re-conventionalized germ-free trout, we identified that this protection is determined by a commensal Flavobacterium strain displaying antibacterial activity against F. columnare. Finally, we demonstrated that use of gnotobiotic trout is a suitable approach for the identification of both endogenous and exogenous probiotic bacterial strains protecting teleostean hosts against F. columnare. This study therefore establishes an ecologically-relevant gnotobiotic model for the study of host-pathogen interactions and colonization resistance in farmed fish. 

Retracted: No

PubPeer comments:
 This article represents a seminal work in the field of host-microbe studies in finfish, particularly salmonids. However, figure 6 seems a bit problematic. Panel B and the rightmost panel C are seemingly identical. ,
High-risk human papillomavirus E6 oncoproteins interact with 14-3-3ζ in a PDZ binding motif-dependent manner
Authors: Siaw Shi Boon
Lawrence Banks
Journal: Journal of Virology (2013)
Discipline: MICROBIOLOGY
Keywords: Cervical cancer; human papillomavirus (HPV); E6 oncoproteins; PDZ binding motif (PBM); protein kinase A (PKA)
Affiliations: International Centre for Genetic Engineering and Biotechnology, Padriciano, Trieste, Italy.

Abstract:  Cervical cancer develops through the combined activities of the human papillomavirus (HPV) E6 and E7 oncoproteins. A defining characteristic of E6 oncoproteins derived from cancer-causing HPV types is the presence of a PDZ binding motif (PBM) at the extreme carboxy terminus of the protein which is absent from E6 proteins derived from the so-called low-risk HPV types. Within this PBM is also a protein kinase A (PKA) phospho-acceptor site, which is thought to negatively regulate the association of E6 with its PDZ domain-containing substrates. We can now show that phosphorylation of E6 by PKA and/or AKT confers the ability to interact with 14-3-3ζ. The interaction is direct and specific for the high-risk HPV E6 oncoproteins, although there are significant differences in the efficiencies with which HPV-16, HPV-18, and HPV-31 E6 oncoproteins can associate with 14-3-3ζ; this correlates directly with their respective susceptibilities to phosphorylation by PKA and/or AKT. We demonstrate here that the interaction between E6 and 14-3-3ζ also requires integrity of the E6 PBM, and downregulation of 14-3-3ζ results in a marked reduction in the levels of HPV-18 E6 expression in HeLa cells. Using phospho-specific anti-E6 antibodies, we also demonstrate significant levels of E6 phosphorylation in vivo. These studies redefine the potential relevance of the E6 PBM in the development of cervical cancer, suggesting that interaction with 14-3-3ζ, as well as the more well-established interactions with PDZ domain-containing substrates, is likely to be responsible for the biological activities attributed to this region of the high-risk HPV E6 oncoproteins. 

Retracted: No

PubPeer comments:
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 #1 Figure 6C. Splices in some panels not present in other panels. Figure 7A. Horizontal change in background in right lane not present in left lane. ![file] ,
Cockayne syndrome A and B proteins differentially regulate recruitment of chromatin remodeling and repair factors to stalled RNA polymerase II in vivo
Authors: Albert A van Zeeland
Leon H F Mullenders
Wim Vermeulen
Maria Fousteri
Journal: Molecular Cell (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Retraction; Data manipulation; Scientific integrity; Investigation; Duplications
Affiliations: Department of Toxicogenetics, Leiden University Medical Center, Einthovenweg 20, 2333 RC Leiden.

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 editors. Molecular Cell has retracted this article following the results of an investigation carried out by Leiden University Medical Center's Committee of Scientific Integrity, which concluded that unacceptable data manipulation by the first author Maria Fousteri led to breaches of scientific integrity, making these results unreliable. These manipulations include duplications (Figures 1C, 2A, 3D [CSB panel], and 5C [p300 panel]), image tilt correction (Figure 4D [CSB panel]), and aesthetic corrections. Additional details can be found in the redacted version of the investigation report (https://www.lumc.nl/cen/att/80813053317221/1263833/report-lumc-committee-scientific-integrity). 

Retracted: Yes

PubPeer comments:
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 In 2015, Leiden University asked the journal to retract this and another paper after an internal investigation. https: www.lumc.nl cen att 80813053317221 1263833 report-lumc-committee-scientific-integrity Three years later, neither paper has been retracted yet. The ERC are currently funding the first author with the 2012-2018 grant TRANSARREST. The embedded table illustrates that there is a growing problem for retractions associated with ERC grant holders. It is something that the ERC might need to concern itself with at some point. ![image] , 
 Supplemental Fig. S2A: More similar than expected ![file] , 
 Retraction Notice to: Cockayne Syndrome A and B Proteins Differentially Regulate Recruitment of Chromatin Remodeling and Repair Factors to Stalled RNA Polymerase II In Vivo https: www.cell.com molecular-cell fulltext S1097-2765(21)01011-X#relatedArticles (Molecular Cell 23, 471u2013482; August 18, 2006) Molecular Cell has retracted this article following the results of an investigation carried out by Leiden University Medical Centeru2019s Committee of Scientific Integrity, which concluded that unacceptable data manipulation by the first author Maria Fousteri led to breaches of scientific integrity, making these results unreliable. These manipulations include duplications (Figures 1C, 2A, 3D [CSB panel], and 5C [p300 panel]), image tilt correction (Figure 4D [CSB panel]), and aesthetic corrections. Additional details can be found in the redacted version of the investigation report . The journal sincerely apologizes to the scientific community for any inconvenience caused by the publication and retraction of this article. ,
Differential involvement of the actin cytoskeleton in differentiation and mitogenesis of thyroid cells: inactivation of Rho proteins contributes to cyclic adenosine monophosphate-dependent gene expression but prevents mitogenesis
Authors: Pierre P Roger
Sara Blancquaert
Klaus Aktories
Jacques E Dumont
Sarah Dremier
Carine Maenhaut
Nathalie Fortemaison
Journal: Endocrinology (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Thyroid epithelial cells; TSH; cAMP; actin stress fiber disruption; differentiation genes
Affiliations: Institute of Interdisciplinary Research, Université Libre de Bruxelles, Belgium.

Abstract:  In thyroid epithelial cells, TSH via cAMP induces a rounding up of the cells associated with actin stress fiber disruption, expression of differentiation genes and cell cycle progression. Here we have evaluated the role of small G proteins of the Rho family and their impact on the actin cytoskeleton in these different processes in primary cultures of canine thyrocytes. TSH and forskolin, but not growth factors, rapidly inactivated RhoA, Rac1, and Cdc42, as assayed by detection of GTP-bound forms. Using toxins that inactivate Rho proteins (toxin B, C3 exoenzyme) or activate them [cytotoxic necrotizing factor 1 (CNF1)], in comparison with disruption of the actin cytoskeleton by dihydrocytochalasin B (DCB) or latrunculin, two unexpected conclusions were reached: 1) inactivation of Rho proteins by cAMP, by disorganizing actin microfilaments and inducing cell retraction, could be necessary and sufficient to mediate at least part of the cAMP-dependent induction of thyroglobulin and thyroid oxidases, but only partly necessary for the induction of Na(+)/I(-) symporter and thyroperoxidase; 2) as indicated by the effect of their inhibition by toxin B and C3, some residual activity of Rho proteins could be required for the induction by cAMP-dependent or -independent mitogenic cascades of DNA synthesis and retinoblastoma protein (pRb) phosphorylation, through mechanisms targeting the activity, but not the stimulated assembly, of cyclin D3-cyclin-dependent kinase 4 complexes. However, at variance with current concepts mostly derived from fibroblast models, DNA synthesis induction and cyclin D3-cyclin-dependent kinase 4 activation were resistant to actin depolymerization by dihydrocytochalasin B in canine thyrocytes, which provides a first such example in a normal adherent cell. 

Retracted: No

PubPeer comments:
 Figure 1 | XRD patterns of CuO-MnO2 nanocomposites obtained at different time. 24h and 48h patterns identical ![file] ,
Vpr-binding protein antagonizes p53-mediated transcription via direct interaction with H3 tail
Authors: Kyunghwan Kim
Kyu Heo
Yue Xiong
Sarah Jackson
Hyunjung Kim
Jongkyu Choi
Woojin An
Journal: Molecular and Cellular Biology (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: VprBP; p53; transcription; apoptosis; nucleosomes
Affiliations: Department of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern California Keck School of Medicine, Los Angeles, California, USA.

Abstract:  HIV-1 Vpr-binding protein (VprBP) has been implicated in the regulation of both DNA replication and cell cycle progression, but its precise role remains unclear. Here we report that VprBP regulates the p53-induced transcription and apoptotic pathway. VprBP is recruited to p53-responsive promoters and suppresses p53 transactivation in the absence of stress stimuli. To maintain target promoters in an inactive state, VprBP stably binds to nucleosomes by recognizing unacetylated H3 tails. Promoter-localized deacetylation of H3 tails is a prerequisite for VprBP to tether and act as a bona fide inhibitor at p53 target genes. VprBP knockdown leads to activation of p53 target genes and causes an increase in DNA damage-induced apoptosis. Moreover, phosphorylation of VprBP at serine 895 impairs the ability of VprBP to bind H3 tails and to repress p53 transactivation. Our results thus reveal a new role for VprBP in regulation of the p53 signaling pathway, as well as molecular mechanisms of cancer development related to VprBP misregulation. 

Retracted: No

PubPeer comments:
 July 2017 correction, here: https: mcb.asm.org content 37 15 e00254-17 It reads:  *Page 787, Fig. 2C, top: Lanes 7 to 12 are erroneous duplications of lanes 1 to 6. We had performed this experiment in triplicate, and the errors occurred when we were copying data to construct the final figure. The corrected panel is given below. The interpretation of the results and findings of our investigations remain unchanged. We sincerely regret our error and apologize for any confusion this may have caused.* Here is the original Figure 2C, with the duplicated panels marked with red boxes. ![file] I thank the authors for correcting this error. This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long ,
<p>PVT1 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer via Regulating miR-148/RAB34 Signal Axis</p>
Authors: Bengtong Yu
Chenghua Jin
Lijie Wang
Yong Xi
Weiyu Shen
Journal: OncoTargets and Therapy (2020)
Discipline: CLINICAL MEDICINE
Keywords: NSCLC; PVT1; RAB34; miR-148; migration
Affiliations: Department of Thoracic Surgery, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo, Zhejiang 315040, People's Republic of China., Department of Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, People's Republic of China.

Abstract:  Objective: It has been verified that long non-coding RNAs (lncRNAs) play critical roles in the development of human cancers. Increasing evidence indicates that lncRNA human plasmacytoma variant translocation1 (PVT1) was dysregulated in non-small cell lung cancer (NSCLC) which is the leading cause of cancer-related death. However, the precise mechanism underlying the effect of PVT1 remains elusive. Our research focused on the correlation of PVT1 to miR-148 and RAB34 in NSCLC. Methods: The quantitative real-time PCR (qRT-PCR) and western blot assay were used to detect gene and protein expression in NSCLC tissues and cells. CCK8, colony formation, transwell and wound healing assays were performed to evaluate the cell function of NSCLC cells. Dual-luciferase activity assay and RNA pull down assays were performed to verify the interaction between miR-148 and its targets. A xenograft test was conducted to detect the impact of RAB34 on tumor development in vitro. Results: In NSCLC tissues and cells, PVT1 and RAB34 were up-regulated, and miR-148 was down-regulated. Overexpression of PVT1 was capable of promoting NSCLC cell proliferation and migration which could be reversed by miR-148 restoration or RAB34 knock down. Also, our data firstly determined that the down-regulation of RAB34 had inhibitor effects while the up-regulation of RAB34 had promotive effects on tumor growth in vitro and in vivo. Conclusion: Those findings indicated that the signal pathway PVT1/miR-148/RAB34 play critical roles in the progression of NSCLC could be proposed in NSCLC as a possible diagnosis or therapeutic targets. 

Retracted: No

PubPeer comments:
 Fig 3E,  wound healing assay , ![file] ,
FBW7 inhibits nucleus pulposus cells proliferation by downregulation of cyclin E in the intervertebral disc degeneration
Authors: J Wang
C-S Feng
J-W Xu
K Yang
H-P Li
H-Y Chen
S Guo
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: FBW7; intervertebral disc degeneration; cell proliferation; collagen II; NP cells
Affiliations: Department of Orthopedics, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. .

Abstract:  Objective: TF-box and WD repeat domain-containing 7 (FBW7), a component of SCF ubiquitin ligase complex, usually acts as a tumor suppressor because it has an ability in the inhibition of cell proliferation. Nevertheless, the role of FBW7 in intervertebral disc degeneration (IDD) is not quite understood. Materials and methods: The total protein and RNA were isolated from patients' disc tissues. WB was carried out to analyze the collagen II and FBW7 protein levels of different Pfirrmann grades disc degeneration. Reverse transcription-polymerase chain reaction (RT-PCR) was used to test the collagen II and FBW7 mRNA expression in these disc samples. NP cells were transfected with siRNA-FWB7 to downregulate the FBW7 expression. SiRNA-NC was used as the sham group. Cyclin E, E2F1, and E2F2 were analyzed with WB and RT-PCR. Results: In this study, different kinds of degenerated disc tissues were analyzed, and it was found that FBW7 was overexpressed in much severe degeneration condition, which was also proved by the IL-1β stimuli nucleus pulposus (NP) cells degeneration model in vitro. Interestingly, the results showed that FBW7 suppression could reverse the degeneration of NP cells. Furthermore, we found that FBW7 induced NP cell cycle arrest in the G1 phase of and inhibited cell proliferation by upregulating p27 expression in vitro. The overexpression of p27 resulted in the inhibition of cyclin E, which promotes cell proliferation. Conclusions: Taken together, our study uncovered that FBW7 played an essential inhibitory role in NP cells proliferation, providing new insights that FBW7 may be a potential strategy for IDD treatments. 

Retracted: No

PubPeer comments:
 Withdrawn. The journal does not provide any details beyond  This article has been withdrawn. The Publisher apologizes for any inconvenience this may cause. , 
 #1 As of the time of writing, the withdrawn paper is still visible here: https: www.europeanreview.org wp wp-content uploads 4591-4598.pdf. Fig 3 displays  Protein expression detected via Western blotting. ![file] Here it is stretched vertically, for comparison with Fig 3 of [Ma et al (2019)] : ![file] Other versions of the loading control are known. Clockwise from upper left: Figure 3 from [Sun et al (2019)] .  NF-u03baB protein expression determined through Western blotting ; [Fig 3 from Long et a (2019)] ; Fig 4 from [Lou et al (2019)] ; and Figure 5 from [Pan et al (2019)] . ![] ,