PReD-Bench/PRed-Bench huggingface dataset:
Overexpression of vimentin contributes to prostate cancer invasion and metastasis via src regulation
Authors: Liangpin Zhao
Qiong Li
Juncheng Wei
Yongtao Zhang
Zhiqiang Han
Ding Ma
Li Meng
Tao Zhu
Mingfu Wu
Yunping Lu
Gang Xu
Gang Chen
Shixuan Wang
Ping Liu
Jianfeng Zhou
Anping Song
Journal: Anticancer research (0)
Discipline: CLINICAL MEDICINE
Keywords: prostate cancer; epithelial-mesenchymal transition; vimentin; invasiveness; metastasis
Affiliations: Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.

Abstract:  A significant proportion of prostate cancer patients treated with curative intent develop advanced disease. At a fundamental biological level, very little is known about what makes the disease aggressive and metastatic. Observational pathology reports and experimental data suggest that an epithelial-mesenchymal transition (EMT) is involved in prostate cancer invasiveness. The mechanism by which vimentin promotes prostate cancer cell invasion and metastasis was examined. The highly metastatic human prostate epithelial cell line PC-3M-1E8 (1E8-H) and the low metastatic line PC-3M-2B4 (2B4-L) were used for comparative proteomic analysis by two-dimensional gel electrophoresis, followed by matrix-assisted laser desorption/time of flight mass spectrometry (MALDI-TOF-MS). A transwell assay was performed to test cell migration and invasion and immunoblotting was used to analyze the relative expression of proteins. High vimentin expression was detected in 1E8-H compared to 2B4-L cells. Down-regulation of vimentin in 1E8-H by antisense-vimentin transfection led to a significant inhibition of invasiveness, and selective stimulation of vimentin activity in 2B4-L by delivery of recombinant vimentin promoted cell invasiveness. Vimentin activity was associated with C-src, beta-catenin and E-cadherin expression. PP2, a specific inhibitor of src family kinases, reduced phospho-beta-catenin expression and induce E-cadherin expression. Vimentin promotes tumor cell invasiveness and the targeting of vimentin/C-src may be a promising strategy for preventing or blocking prostate cancer metastasis. 

Retracted: No

PubPeer comments:
 Retraction, March 2022, found here: https: link.springer.com article 10.1007 s00784-022-04419-8  The Editor in Chief has retracted this article because it contains material that substantially overlaps with the following article [1]. Xianghuai Zheng has agreed to this retraction but not to the wording of this retraction notice. Jianjiang Zhao, Shuguang Liu, Zhiping Wang, Bo Jia and Xi Lin have not responded to any correspondence from the editor publisher about this retraction. Reference [1] Nan Fang Yi Ke Da Xue Xue Baov Journal of Southern Medical University: Zheng Xianghuai, Lin Xi, Chai Jinyou, Qi Rui, Liu Shuguang. Application of digital positioning guide plate in extraction of impacted supernumerary teeth. J South Med Univ, 2020, 40(6): 907-910. https: doi.org 10.12122 j.issn.1673-4254.2020.06.20 ,
The Neuroprotective Role of MiR‚Ä?24‚Ä?p in a 6‚ÄêHydroxydopamine‚ÄêInduced Cell Model of Parkinson's Disease via the Regulation of ANAX5
Authors: Hong-Mei Liu
Bing Zhang
Li-Wen Tai
Rui-Fang Dong
Ning-Ning Liu
Fang-Kun Shi
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: 6-OHDA; ANXA5; PARKINSON'S DISEASE; miR-124-3p.
Affiliations: Department of NeurologyCangzhou Central HospitalCangzhou CityHebei Province 061001China, Department of NeurologyThe First Hospital of ShijiazhuangShijiazhuangHebei Province 050011China, Department of NeurologyThe Second Hospital of Hebei Medical UniversityShijiazhuangHebei Province 050011China

Abstract:  Parkinson's disease (PD), the second most common neurodegenerative disorder, is characterized by a progressive loss of dopaminergic neurons in the midbrain. Several pathogenetic factors have been involved in the onset and progression of PD, including inflammation, oxidative stress, unfolded protein accumulation, and apoptosis. Ample evidence indicates that miRNAs could regulate post-transcriptional gene expression and neuronal disease. In this study, we evaluated the effects and mechanism of miR-124-3p on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in PC12 cells and SH-SY5Y cells. qRT-PCR results showed that the level of miR-124-3p was downregulated in 6-OHDA-treated PC12 and SH-SY5Y cells, and overexpression of miR-124-3p significantly promoted the cell viability of 6-OHDA-treated PC12 and SH-SY5Y cells, whereas miR-124-3p inhibitor reversed these effects. In addition, PC12 or SH-SY5Y cells were treated with miR-124-3p mimics or inhibitors following 6-OHDA administration, which mediated cell apoptosis and downregulation or upregulation of Caspase-3 activity, respectively. A luciferase reporter assay revealed that annexinA5 (ANXA5) is a direct target gene of miR-124-3p, and miR-124-3p overexpression markedly downregulated the level of ANXA5. Strikingly, further analysis showed that miR-124-3p enhanced the viability of 6-OHDA-treated PC12 or SH-SY5Y cells by targeting ANXA5, which was associated with the stimulation of the ERK pathway. This study revealed that miR-124-3p may play a neuroprotective role in PD; this observation may provide new ideas and therapeutic targets for PD. J. Cell. Biochem. 119: 269-277, 2018. ¬© 2017 Wiley Periodicals, Inc. 

Retracted: No

PubPeer comments:
 Brought to my attention by a reader. Figure 7D. The IP:MAD2 MAD2 panel looks similar to the IP:CDC20 CDC20 panel. Shown with red boxes. Below, the figure on the right shows the same blot panels at a higher exposure, to bring out more details. Could the authors please check?  ,
Potential inhibitors of coronavirus 3-chymotrypsin-like protease (3CLpro): an in silico screening of alkaloids and terpenoids from African medicinal plants
Authors: Saheed O Afolabi
Oludare M Ogunyemi
Adegbenro P Adegunloye
Gideon A Gyebi
Olalekan B Ogunro
Journal: Journal of biomolecular structure & dynamics (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: COVID-19; SARS-CoV-2; coronavirus 3CLpro; molecular docking; natural product.
Affiliations: Department of Biological Sciences, Salem University, Lokoja, Nigeria., Department of Biological Sciences, KolaDaisi University, Ibadan, Nigeria., Department of Biochemistry, Faculty of Life Sciences, University of Ilorin, Ilorin, Nigeria., Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, University of Ilorin, Ilorin, Nigeria.

Abstract:  The novel coronavirus disease 2019 (COVID-19) caused by SARS-COV-2 has raised myriad of global concerns. There is currently no FDA approved antiviral strategy to alleviate the disease burden. The conserved 3-chymotrypsin-like protease (3CLpro), which controls coronavirus replication is a promising drug target for combating the coronavirus infection. This study screens some African plants derived alkaloids and terpenoids as potential inhibitors of coronavirus 3CLpro using in silico approach. Bioactive alkaloids (62) and terpenoids (100) of plants native to Africa were docked to the 3CLpro of the novel SARS-CoV-2. The top twenty alkaloids and terpenoids with high binding affinities to the SARS-CoV-2 3CLpro were further docked to the 3CLpro of SARS-CoV and MERS-CoV. The docking scores were compared with 3CLpro-referenced inhibitors (Lopinavir and Ritonavir). The top docked compounds were further subjected to ADEM/Tox and Lipinski filtering analyses for drug-likeness prediction analysis. This ligand-protein interaction study revealed that more than half of the top twenty alkaloids and terpenoids interacted favourably with the coronaviruses 3CLpro, and had binding affinities that surpassed that of lopinavir and ritonavir. Also, a highly defined hit-list of seven compounds (10-Hydroxyusambarensine, Cryptoquindoline, 6-Oxoisoiguesterin, 22-Hydroxyhopan-3-one, Cryptospirolepine, Isoiguesterin and 20-Epibryonolic acid) were identified. Furthermore, four non-toxic, druggable plant derived alkaloids (10-Hydroxyusambarensine, and Cryptoquindoline) and terpenoids (6-Oxoisoiguesterin and 22-Hydroxyhopan-3-one), that bind to the receptor-binding site and catalytic dyad of SARS-CoV-2 3CLpro were identified from the predictive ADME/tox and Lipinski filter analysis. However, further experimental analyses are required for developing these possible leads into natural anti-COVID-19 therapeutic agents for combating the pandemic.Communicated by Ramaswamy H. Sarma. 

Retracted: No

PubPeer comments:
 There is controversy over where the notion that iPS  reprogramming factors can be used to induce rejuvenation without de-differentiation was first put forward and tested (see comments in https: pubpeer.com publications E006ECA3F03CA48839B631F5682C7A. It is this hypothesis that is tested in this work and other recent papers. ,
Robo1-specific CAR-NK Immunotherapy Enhances Efficacy of 125I Seed Brachytherapy in an Orthotopic Mouse Model of Human Pancreatic Carcinoma
Authors: Fenju Liu
Jian Lu
Pang Haopeng
Ning Xia
Zhongmin Wang
J U Gong
Zhijin Chen
Zhijian Yang
Robert M Hoffman
Yunfeng Zheng
Y U Sun
Journal: Anticancer research (2019)
Discipline: CLINICAL MEDICINE
Keywords: 125I seed; CAR-NK; pancreatic cancer.
Affiliations: Department of Radiology, School of Radiation Medicine and Protection, Medical College of Soochow University, School for Radiological and Interdisciplinary Sciences (RAD-X), Soochow University, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, P.R. China., Department of Interventional Radiology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China., Department of Radiobiology, Ruijin Hospital Luwan Branch, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China., Department of Interventional Radiology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China  ., Origin Biosciences Inc., Nanjing, P.R. China., Anticancer Inc, San Diego, CA, U.S.A., Department of Radiology, School of Radiation Medicine and Protection, Medical College of Soochow University, School for Radiological and Interdisciplinary Sciences (RAD-X), Soochow University, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, P.R. China  .

Abstract:  Background/aim: The aim of the current study was to investigate the synergistic efficacy of Robo1 bichimeric antigen receptor-natural killer cell (BiCAR-NK) immunotherapy and 125I seed brachytherapy in an orthotopic pancreatic cancer mouse model. Materials and methods: The orthotopic pancreatic tumor model was established with human pancreatic cancer BxPC-3 cells expressing red fluorescent protein. The mice were treated with 125I seed implantation alone or the combination of 125I seeds with Robo1-specific CAR-NK cells. To assess tumor inhibition, in vivo fluorescence imaging was conducted. 7 Tesla magnetic resonance (7T-MR) scanning was applied to measure the changes in the metabolic profiles of tumor tissues. Results: Tumor size was significantly reduced in the 125I and 125I +CAR-NK treated group compared to the untreated group (p&lt;0.05). The 125I seed +CAR-NK treated group showed significantly higher tumor reduction than 125I seed treatment alone (p&lt;0.05). T1 diffusion weighted imaging (T1DWI) sequence showed that the tumors of the 125I +BiCAR-NK treated group had a significantly higher grey scale value than the tumors from the untreated control and the group treated with 125I seed alone (p&lt;0.05). Conclusion: Robo1 specific CAR-NK immunotherapy enhances efficacy of 125I seed brachytherapy in an orthotopic pancreatic cancer mouse model. 

Retracted: No

PubPeer comments:
 This paper has been corrected twice, but still has an obvious error in Figure 2.  ,
RETRACTED ARTICLE: The fatty liver index (FLI) and incident hypertension: a longitudinal study among Chinese population
Authors: Kena Zhou
Jie Cen
Journal: Lipids in Health and Disease (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Epidemiology; Fatty liver index; Hypertension; Nonalcoholic fatty liver.
Affiliations: Ningbo No. 9 Hospital, Ningbo, 315020, China., Ningbo University, Ningbo, 315020, China., Ningbo No. 9 Hospital, Ningbo, 315020, China. ., Ningbo University, Ningbo, 315020, China. .

Abstract:  Background: Hypertension and nonalcoholic fatty liver both have been considered as the serious public health problems in recent years. However, the longitudinal association between hypertension and nonalcoholic fatty liver remains unclear in Chinese population. Methods: This study was aimed to investigate the longitudinal association between nonalcoholic fatty liver assessed by fatty liver index and the incident hypertension among Chinese population and to evaluate the ability of FLI index, through comparing with the predictive value of other indexes. Results: Four thousand six hundred eighty-six subjects (3177 males and 1509 females) were involved and followed up for 9 years. The subjects were divided into groups according to the fatty liver index. Univariate and multivariate Cox regression models were used to analyze the risk factors of hypertension. After 9 years of follow-up, 2047 subjects developed hypertension. The overall 9-year cumulative incidence of HTN was 43.7%, ranging from 36.0% (FLI &lt; 30) to 75.3% (FLI ‚â?60) (P for trend &lt; 0.001). Cox regression analyses indicated that nonalcoholic fatty liver assessed by fatty liver index was independently and positively associated with the risk of incident hypertension. In receiver operating characteristic (ROC) curve analysis, the ROC curve (AUC) of FLI was 0.701 (95% CI 0.686-0.716), which was larger than that of its components. Conclusion: The nonalcoholic fatty liver assessed by FLI independently predicted the incident hypertension among the Chinese population. 

Retracted: Yes

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A105 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 23 publications have an expression of concern. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
Ras-ERK1/2 Signaling Promotes The Development Of Osteosarcoma By Regulating H2BK12ac Through CBP
Authors: Xianlun Xu
Hao Yu
Yupeng Xu
Journal: Cancer management and research (2019)
Discipline: CLINICAL MEDICINE
Keywords: CBP; H2BK12ac; HDAC1; MDM2; Ras-ERK1/2 signaling
Affiliations: Department of Traumatology, Jining No.1 People's Hospital, Jining 272011, Shandong, People's Republic of China., Affiliated Jining No.1 People's Hospital of Jining Medical University, Jining Medical University, Jining 272067, Shandong, People's Republic of China., Department of Orthopedics, Jining Bone Fracture Hospital, Jining 272000, Shandong, People's Republic of China.

Abstract:  Background: H2BK12ac is an important histone acetylation pattern of H2B, which has been reported in several cancers. However, whether H2BK12ac joins in Ras-ERK1/2 activation-induced osteosarcoma (OS) cell behaviors remain unclear. The study explored this peradventure and revealed the underlying mechanism. Methods: MG-63 cells were transfected with pEGFP-N1, pEGFP-RasWT and pEGFP-K-RasG12V/T35S, H2BK12ac and ERK1/2 expression levels were analyzed by Western blot. Effects of H2BK12ac on cell viability, migration, colony formation and cell cycle were investigated by MTT, Transwell, soft-agar colony formation and flow cytometry assays. RT-qPCR and ChIP were performed to study the effect of H2BK12ac and CBP on ERK1/2-downstream gene transcriptions. Results: H2BK12ac was specifically down-regulated by Ras-ERK1/2 activation in MG-63 cells. Down-regulated H2BK12ac participated in regulating cell proliferation and migration of MG-63 cells, meanwhile, affected the transcription of ERK1/2-downstream genes. Additionally, silence of HDAC1 up-regulated H2BK12ac expression, and inhibited the promoting effect of Ras-ERK1/2 on MG-63 cells' proliferation, migration and RNA expression levels of ERK1/2-downstream genes. Further, the degradation of CBP mediated by MDM2 was discovered to be linked to Ras-ERK1/2 activation-induced H2BK12ac down-regulation. Conclusion: These findings from the study demonstrated that Ras-ERK1/2 signaling could promote the development of OS via regulating H2BK12ac through MDM2-mediated CBP degradation. 

Retracted: No

PubPeer comments:
 Figure 2. Much more similar than you would expect. https: imgur.com dLxDFwR ,
The SWI/SNF chromatin remodeling complex helps resolve R-loop-mediated transcription‚Äìreplication conflicts
Authors: Sergio Mu√±oz
Andr√©s Aguilera
Sonia Barroso
Aleix Bayona-Feliu
Journal: Nature Genetics (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ATP-dependent chromatin remodelers; human cancer; SWI/SNF complexes; cBAF; ncBAF
Affiliations: Centro Andaluz de Biolog√≠a Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, Seville, Spain., Departamento de Gen√©tica, Facultad de Biolog√≠a, Universidad de Sevilla, Seville, Spain., Centro Andaluz de Biolog√≠a Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, Seville, Spain. ., Departamento de Gen√©tica, Facultad de Biolog√≠a, Universidad de Sevilla, Seville, Spain. .

Abstract:  ATP-dependent chromatin remodelers are commonly mutated in human cancer. Mammalian SWI/SNF complexes comprise three conserved multisubunit chromatin remodelers (cBAF, ncBAF and PBAF) that share the BRG1 (also known as SMARCA4) subunit responsible for the main ATPase activity. BRG1 is the most frequently mutated Snf2-like ATPase in cancer. In the present study, we have investigated the role of SWI/SNF in genome instability, a hallmark of cancer cells, given its role in transcription, DNA replication and DNA-damage repair. We show that depletion of BRG1 increases R-loops and R-loop-dependent DNA breaks, as well as transcription-replication (T-R) conflicts. BRG1 colocalizes with R-loops and replication fork blocks, as determined by FANCD2 foci, with BRG1 depletion being epistatic to FANCD2 silencing. Our study, extended to other components of SWI/SNF, uncovers a key role of the SWI/SNF complex, in particular cBAF, in helping resolve R-loop-mediated T-R conflicts, thus, unveiling a new mechanism by which chromatin remodeling protects genome integrity. 

Retracted: No

PubPeer comments:
 Based on recent Smolka et al. study , a lot of the microscopy data in this study could be artifacts. The preprint has been around since January 2020. ,
hnRNP K: an HDM2 target and transcriptional coactivator of p53 in response to DNA damage
Authors: Philip Masterson
Stephen P Jackson
Abdeladim Moumen
Mark J O&#x27;Connor
Journal: Cell (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: DNA damage; p53-dependent transcriptional induction; hnRNP K; proteomics; ATM
Affiliations: The Wellcome Trust and Cancer Research UK Gurdon Institute and Department of Zoology, Cambridge University, Tennis Court Road, Cambridge CB2 1QN, United Kingdom.

Abstract:  In response to DNA damage, mammalian cells trigger the p53-dependent transcriptional induction of factors that regulate DNA repair, cell-cycle progression, or cell survival. Through differential proteomics, we identify heterogeneous nuclear ribonucleoprotein K (hnRNP K) as being rapidly induced by DNA damage in a manner that requires the DNA-damage signaling kinases ATM or ATR. Induction of hnRNP K ensues through the inhibition of its ubiquitin-dependent proteasomal degradation mediated by the ubiquitin E3 ligase HDM2/MDM2. Strikingly, hnRNP K depletion abrogates transcriptional induction of p53 target genes and causes defects in DNA-damage-induced cell-cycle-checkpoint arrests. Furthermore, in response to DNA damage, p53 and hnRNP K are recruited to the promoters of p53-responsive genes in a mutually dependent manner. These findings establish hnRNP K as a new HDM2 target and show that, by serving as a cofactor for p53, hnRNP K plays key roles in coordinating transcriptional responses to DNA damage. 

Retracted: No

PubPeer comments:
 Figure 1. Much more similar than expected.  , 
 Figures 1E, 1F, and 3A. Much more similar than expected, although the conditions, cells are different.  , 
 Figure 7B. Much more similar than expected.  , 
 WB Alpha-K in figure 7A very similar to Tubulin WB in figures 1E, 1F and 3A.  , 
 Figure 4E. Much more similar than expected.  , 
 Figure 4A. Horizontal flip WB alpha-HDM2 very similar to Tub WB figures 1E, 1F and 3A, and also similar to WB alpha-K in figure 7A.  , 
 Much more similar than expected.  , 
 Figure 4B. Much more similar after horizontal flip and vertical compression than expected.  , 
 Figures 4B and 4D. Much more similar after horizontal compression than expected, even though the cells are different.  , 
 #3 Figure 7A. Much more similar after 180 degree rotation than expected.  , 
 Figure 1E. Much more similar after vertical stretch than expected.  , 
 Senior author. https: retractionwatch.com 2019 04 11 authors-have-papers-in-nature-and-science-retracted-on-the-same-day ,
Ferruginol Diterpenoid Selectively Inhibits Human Thyroid Cancer Growth by Inducing Mitochondrial Dependent Apoptosis, Endogenous Reactive Oxygen Species (ROS) Production, Mitochondrial Membrane Potential Loss and Suppression of Mitogen-Activated Protein Kinase (MAPK) and PI3K/AKT Signaling Pathways
Authors: Ningdong Hu
Jingjing Zhou
Xu Xia
Guoqing Luo
Haibo Zhou
Guanjie Li
Journal: Medical Science Monitor (2019)
Discipline: CLINICAL MEDICINE
Keywords: Thyroid cancer; chemotherapy; ferruginol; antiproliferative; apoptosis
Affiliations: Department of Cardiothoracic Surgery, Qingyuan People's Hospital (The Sixth Affiliated Hospital of Guangzhou Medical University), Qingyuan, Guangdong, China (mainland).

Abstract:  BACKGROUND Thyroid cancer causes considerable mortality and morbidity across the globe. Owing to the unavailability of biomarkers and the adverse effects of existing drugs, there is an urgent need to develop efficient chemotherapy for the treatment of thyroid cancers. Plants have served as exceptional source of drugs for the treatment of lethal diseases. The purpose of this study was to evaluate the anticancer effects of ferruginol against thyroid cancer cells. MATERIAL AND METHODS We monitored the cell proliferation rate using 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was detected using 4',6-diamidino-2-phenylindole (DAPI), acridine orange/ethidium bromide (AO/EB), and annexin V/propidium iodide (PI) staining. Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) levels were examined by fluorescence microscopy. Protein expressed was examined by western blotting. RESULTS We found that ferruginol exerted potent antiproliferative action against thyroid cancer cells, and an IC‚ÇÖ‚ÇÄ of 12 ¬µM was observed for ferruginol against the MDA-T32 cell line. The toxic effects of ferruginol were less pronounced against normal cells. The anticancer effects of ferruginol were likely due to the induction of apoptosis which was also associated with upregulation of Bax and downregulation of Bcl-2. Ferruginol also caused ROS mediated alterations in the MMP of MDA-T32 cells. In MDA-T32 cells, ferruginol might also block the MAPK and PI3K/AKT signaling pathway, which is believed to be an important therapeutic target of anticancer drugs. CONCLUSIONS In conclusion, in view of the results of this study, it might be suggested that ferruginol might serve as an essential lead molecule for the treatment of thyroid cancer provided further in-depth studies especially studying ferruginol toxicological as well as in vivo studies are needed. 

Retracted: Yes

PubPeer comments:
 Figure 2G. * Yellow boxes: Two panels appear to show an overlap.  Also, the corresponding email address does not appear to match the name of the corresponding author: Yan Zhang, Email: yinwu84714447@163.com ,
MicroRNA-215 enhances invasion and migration by targeting retinoblastoma tumor suppressor gene 1 in high-grade glioma
Authors: Jianjing Sun
Yuzhen Wei
Xingang Li
Journal: Biotechnology Letters (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Glioma; Invasion; Migration; Retinoblastoma tumor suppressor gene 1; miRNA-215.
Affiliations: Department of Neurosurgery, Qilu Hospital of Shandong University, 107 of Wenhua Xi Road Lixia District, Jinan, 250012, Shandong, People's Republic of China., Department of Neurosurgery, Jining No.1 People's Hospital, Jining, Shandong, People's Republic of China., Department of Endocrinology, Jining No.1 People's Hospital, Jining, 272 011, Shandong, People's Republic of China., Department of Neurosurgery, Qilu Hospital of Shandong University, 107 of Wenhua Xi Road Lixia District, Jinan, 250012, Shandong, People's Republic of China. ., Brain Science Research Institute, Shandong University, Jinan, Shandong, People's Republic of China. .

Abstract:  Objective: To elucidate the molecular mechanism of microRNA-215 (miR-215) in the migration and invasion of high grade glioma. Results: 42 Patients were analysed for clinicopathological characteristics. qRT-PCR showed that miR-215 was up-regulated in glioma tissues compared with non-neoplastic brain tissues (P &lt; 0.05). The up-regulated miR-215 was closely associated with high grade glioma (P &lt; 0.01) and poor overall survival (P &lt; 0.01). Transwell assay showed that re-expression of miR-215 enhanced migration and invasion of glioma cells. miR-215 also down-regulated retinoblastoma tumor suppressor gene 1 (RB1) expression by targeting its 3'-UTR. Reversely, re-expression of RB1 inhibited partial effect of miR-215 on migration and invasion in vitro. Conclusions: Re-expression of miR-215 promoted cell migration and invasion of glioma by targeting RB1. miR-215 can thus be used as a biomarker for tumor progression and prognosis in human high grade glioma. 

Retracted: No

PubPeer comments:
 Figure 4B had an overlap, involving scaling up or down, unlikely by accident  , 
 There are more serious trouble in this paper, where microscopy data has been reused and presented as something else.  , 
 #2 Indeed.  , 
 Retracted [23 July 2022] . -----------------------------  The Editors in Chief have retracted this article at the authoru2019s request. After publication, significant concerns regarding a number of Figures presented in this work, which question the integrity of the data. The Editors in chief, therefore, no longer have confidence in the results of this study. Xingang Li was not involved in this study and was not aware of its publication. All authors agree to this retraction. ,
Overexpression of EIF5A2 promotes colorectal carcinoma cell aggressiveness by upregulating MTA1 through C-myc to induce epithelial‚Äìmesenchymaltransition
Authors: Shi-Juan Mai
Sui-Sui Dong
Marie C Lin
Hsiang-Fu Kung
Wei Zhu
Zhu-Ting Tong
Yi-Ji Liao
Xin-Yuan Guan
Mu-Yan Cai
Yi-Xin Zeng
Xiu-Wu Bian
Dan Xie
Journal: Gut (2012)
Discipline: CLINICAL MEDICINE
Keywords: EIF5A2; colorectal carcinoma; aggressiveness; metastasis; survival
Affiliations: State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, Guangzhou, China.

Abstract:  Background and aims: The authors have previously isolated a putative oncogene, eukaryotic initiation factor 5A2 (EIF5A2) from 3q26. In this study, EIF5A2 was characterised for its role in colorectal carcinoma (CRC) aggressiveness and underlying molecular mechanisms. Methods: The expression dynamics of EIF5A2 were examined by immunohistochemistry in a cohort of carcinomatous and non-neoplastic colorectal tissues and cells. A series of in-vivo and in-vitro assays was performed to elucidate the function of EIF5A2 in CRC and its underlying mechanisms. Results: The overexpression of EIF5A2 was examined by immunohistochemistry in 102/229 (44.5%) CRC patients, and it was significantly correlated with tumour metastasis and determined to be an independent predictor of shortened survival (p&lt;0.05). Ectopic overexpression of EIF5A2 in CRC cells enhanced cell motility and invasion in vitro and tumour metastasis in vivo, and induced epithelial-mesenchymal transition (EMT). The depletion of EIF5A2 expression prevented CRC cell invasiveness and inhibited EMT. Importantly, the metastasis-associated protein 1 (MTA1) gene was identified as a potential downstream target of EIF5A2 in CRC cells, and knockdown of MTA1 eliminated the augmentation of carcinoma cell migration, invasion and EMT by ectopic EIF5A2. The overexpression of EIF5A2 in CRC cells substantially enhanced the enrichment of c-myc on the promoter of MTA1, and MTA1 upregulation by EIF5A2 was partly dependent on c-myc. Conclusion: The data suggest that EIF5A2 plays an important oncogenic role in CRC aggressiveness by the upregulation of MTA1 to induce EMT, and EIF5A2 could be employed as a novel prognostic marker and/or effective therapeutic target for CRC. 

Retracted: No

PubPeer comments:
 Figure 6D contains two images which appear to overlap.  ,
Exploring the potential role of disease-causing mutation in a gene desert: duplication of noncoding elements 5' of GRIA3 is associated with GRIA3 silencing and X-linked intellectual disability
Authors: Christel Thauvin-Robinet
Alice Masurel-Paulet
Christophe Philippe
C√©line Bonnet
Philippe Jonveaux
Francine Mugneret
Asma Ali Khan
Laurence Faivre
Patrick Callier
Myl√®ne B√©ri-Dexheimer
Journal: Human Mutation (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: GRIA3; intellectual disability; epilepsy; duplication; gene desert
Affiliations: Laboratoire de G√©n√©tique, EA 4368, Nancy Universit√©, Centre Hospitalier Universitaire de Nancy, France.

Abstract:  GRIA3 encodes glutamate receptor ionotropic AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) subunit 3 and has been previously involved in X-linked intellectual disability (ID). We report on a male proband with ID and epilepsy associated with a duplication mapping within a gene desert, 874-kb upstream of the GRIA3 gene. This 970-kb duplication is maternally inherited. The proband's mother has a skewed X chromosome-inactivation pattern in agreement with her normal cognitive function. Quantitative polymerase chain reaction analysis indicates absence of GRIA3 mRNA in the proband lymphocytes relative to a wild-type control. Centromeric to the duplicated region, comparative genomic analysis showed a 2268-bp evolutionarily conserved region that could be a critical transcription factor binding-site for GRIA3 expression. The repositioning of distant-acting sequences, rather a missense/nonsense mutation, is considered to be causative for GRIA3-linked ID. This study illustrates the importance of high-resolution array-Comparative Genomic Hybridization analysis in exploring the potential role of disease-causing mutation in functional noncoding sequences. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: onlinelibrary.wiley.com doi 10.1002 humu.23991 Retraction: Bonnet et al., Exploring the potential role of diseaseu2010causing mutation in a gene desert: duplication of noncoding elements 5u2019 of GRIA3 is associated with GRIA3 silencing and Xu2010linked intellectual disability, Human Mutation 2012, 33 (2) 335u2013358 . The above article, first published online on 28 November 2011 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement with the authors, the journal Editoru2010inu2010Chief Garry R. Cutting, and Wiley Periodicals, Inc. The retraction has been agreed due to subsequent evidence presented by the authors (Thevenon et al. 2014, Am J Hum Genet 95(1):113u2010120. https: doi.org 10.1016 j.ajhg.2014.06.006) that the original reported observation of duplicated noncoding elements 5u2019 of the Xu2010linked GRIA3 gene was in fact not associated with the observed phenotype. The authors sincerely apologize and in view of correcting the literature, they requested to retract this article. The article was initially retracted in June 2016, but without a retraction statement, which has been added to the publication record as of February 2020. The publisher regrets the error. ,
A Synthetic Curcuminoid Analog, (2E,6E)-2,6-bis(2-(trifluoromethyl)benzylidene)cyclohexanone, Ameliorates Impaired Wound Healing in Streptozotocin-Induced Diabetic Mice by Increasing miR-146a
Authors: Tianhui You
Jingjuan Huang
Rui Wang
Bing Liu
Jia Fu
Journal: Molecules (2020)
Discipline: CHEMISTRY
Keywords: NF-Œ∫B; curcuminoid; inflammation; miR-146a; synthetic analog
Affiliations: School of Nursing, Guangdong Pharmaceutical University, Guangzhou 510006, China., Guangzhou Key Laboratory of Construction and Application of New Drug Screening Model Systems, Guangdong Pharmaceutical University, Guangzhou 510006, China., Key Laboratory of New Drug Discovery and Evaluation of Ordinary Universities of Guangdong Province, Guangdong Pharmaceutical University, Guangzhou 510006, China., School of Pharmacy, Guangdong Pharmaceutical University, Guangzhou 510006, China., Guangdong Key Laboratory of Pharmaceutical Bioactive Substances, Guangdong Pharmaceutical University, Guangzhou 510006, China.

Abstract:  The impairment in diabetic wound healing represents a significant clinical problem, with no efficient targeted treatments for these wound disorders. Curcumin is well confirmed to improve diabetic wound healing, however, its low bioavailability and poor solubility severely limit its clinical application. This study aims to provide the pharmacological basis for the use of (2E,6E)-2,6-bis(2-(trifluoromethyl)benzylidene)cyclohexanone (C66). The results showed that topically applied C66 improved cutaneous wound healing in vivo. Further studies showed that C66 treatment increased the level of microRNA-146a (miR-146a) in the wounds in streptozotocin (STZ)-induced diabetic mice, downregulated the expression of interleukin-1 receptor-associated kinase 1 (IRAK1) and phosphorylated nuclear factor-Œ∫B (NF-Œ∫B) p65 subunit (p-p65) (both p &lt; 0.05), and suppressed the mRNA expression of inflammation-related cytokines, tumor necrosis factor-Œ± (TNF-Œ±), interleukin-8 (IL-8), and interleukin-6 (IL-6). The in vitro data obtained in human umbilical vein endothelial cells (HUVECs) showed that C66 could reverse high glucose (HG)-induced NF-Œ∫B activation due to upregulation of miR-146a expression, which matched the in vivo findings. In conclusion, the present study indicates that C66 exerts anti-inflammation activity and accelerates skin wound healing of diabetic mice, probably via increasing miR-146a and inhibiting the NF-Œ∫B-mediated inflammation pathway. Therefore, C66 may be a promising alternative for the treatment of diabetic wounds. 

Retracted: No

PubPeer comments:
 Fig 1c.  Pathological observation of IA tissues and normal arterial tissues by HE staining .  Normal arterial tissue is not normal.   Intracranial aneurysm tissue is even more abnormal, with the lower edge repeated (after a flip and a rotation) as the right-hand edge. , 
 Fig 2 c,d,e. None of these panels were designed to survive close scrutiny.  Some examples.  , 
  We would like to acknowledge the reviewers for their helpful comments on this pap. ,
ATM-dependent phosphorylation of heterogeneous nuclear ribonucleoprotein K promotes p53 transcriptional activation in response to DNA damage
Authors: Katherine L Dry
Stephen P Jackson
Christine Magill
Abdeladim Moumen
Journal: Cell Cycle (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ATM; DNA damage; p53; phosphorylation; transcription.
Affiliations: DNA Damage Response Group, Basic Medical Science Department, St. George's University of London, London, UK.

Abstract:  Previous work has established that heterogeneous nuclear ribonucleoprotein K (hnRNP K) is stabilized in an ATM-dependent manner in response to DNA damage and acts as a cofactor for p53-mediated transcription. Here, we show that in response to DNA damage caused by ionizing radiation, hnRNP K is phosphorylated in an ATM-dependent manner. Furthermore, our data indicate that ATM-dependent hnRNP K phosphorylation is required for its stabilization and its function as a p53 transcriptional cofactor in response to DNA damage. These findings thereby establish hnRNP K as an ATM target and help define how ATM orchestrates p53-dependent transcriptional responses in response to genotoxic stress. 

Retracted: No

PubPeer comments:
 Figure 1A. Much more similar than exepcted.  , 
 Figure 3B. Splice between rightmost lanes in hnRNP panel, but no splice in p21 WAF1 panel. Band rightmost Tubulin lane is a step down compared with all the other bands in that panel and there is no general background.  , 
 Figure 1B. Much more similar than expected.  , 
 Senior author. https: retractionwatch.com 2019 04 11 authors-have-papers-in-nature-and-science-retracted-on-the-same-day ,
MicroRNA‚Ä?08a directly targets Src kinase signaling inhibitor 1 to facilitate cell proliferation and invasion in non‚Äësmall cell lung cancer
Authors: Wuzhang Wang
Li Liu
Xiuwen Wang
Song Gao
Journal: Molecular Medicine Reports (2019)
Discipline: CLINICAL MEDICINE
Keywords: miR-208a; non-small cell lung cancer; oncogenic functions; SRCIN1; ERK signaling pathway
Affiliations: Department of Chemotherapy, Cancer Center, Qilu Hospital of Shandong University, Jinan, Shandong 250012, P.R. China, Minimally Invasive Interventional Diagnosis and Treatment Ward, Shandong Chest Hospital, Jinan, Shandong 250013, P.R. China

Abstract:  The abnormal expression of microRNAs (miRNAs/miRs) has a critical function in the formation and progression of non‚Äësmall cell lung cancer (NSCLC). Therefore, understanding the association between NSCLC and dysregulated miRNAs may allow for the identification of novel diagnostic and therapeutic biomarkers for patients with this malignancy. Previous studies have validated miR‚Ä?08a as a cancer‚Äëassociated miRNA in multiple different types of human cancer, however, its expression pattern and precise function in NSCLC remains yet to be elucidated. Therefore, the aims of the present study were to measure miR‚Ä?08a expression in NSCLC, investigate its specific functions in NSCLC and determine its exact regulatory mechanisms. Herein, the results demonstrated that miR‚Ä?08a was significantly upregulated in NSCLC tissues and cell lines compared with that in adjacent non‚Äëcancerous tissues and a non‚Äëtumorigenic bronchial epithelium BEAS‚Ä?B cell line (P&lt;0.05, respectively). The high expression level of miR‚Ä?08a exhibited an obvious association with Tumor‚ÄëNode‚ÄëMetastasis stage and lymph node metastasis. MiR‚Ä?08a silencing decreased the proliferative and invasive capacities of NSCLC cells. Notably, Src kinase signaling inhibitor 1 (SRCIN1) was verified as a potential direct target gene of miR‚Ä?08a in NSCLC cells. Furthermore, SRCIN1 knockdown was able to rescue the miR‚Ä?08a‚Äëmediated effects on NSCLC cells. In addition to this, silencing miR‚Ä?08a expression inhibited the extracellular regulated kinase (ERK) signaling pathway in NSCLC. Overall, to the best of our knowledge, the present study is the first to provide evidence that miR‚Ä?08a exerts oncogenic functions in the carcinogenesis and progression of NSCLC by directly targeting SRCIN1 and regulating the ERK pathway. Therefore, miR‚Ä?08a may be developed as a potential target for treating patients with NSCLC. 

Retracted: No

PubPeer comments:
 Figs 3E,  (E) protein expression levels in the indicated cell lines ; 4A,  Western blot analysis was performed to examine SRCIN1 protein expression levels in the differently treated cells 72 h following transfection ;  miRu2011208a affects the ERK signaling pathway in NSC .  Western Blots of this stylised appearance are frequent in the products of the [ Direct target papermill] . (e.g.) Figs 7B E F, 1C from [Ouyang et al (2020)] ;  WBs from [Wang et al (2019)] **[retracted]**;  Figs 2E F, 5A, 6A from [Xia et al (2020)] ;:  ,
Identification of methylated deoxyadenosines in vertebrates reveals diversity in DNA modifications
Authors: Christian Frezza
George E Allen
Magdalena J Koziol
John B Gurdon
Ana S H Costa
Charles R Bradshaw
Journal: Nature structural & molecular biology (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Methylation; 5-methylcytosine; N(6)-methyldeoxyadenosine; epigenetic mark; vertebrate DNA
Affiliations: Wellcome Trust Cancer Research UK Gurdon Institute, University of Cambridge., Department of Zoology, University of Cambridge., Medical Research Cancer Unit, University of Cambridge, Hutchison/MRC Research Centre.

Abstract:  Methylation of cytosine deoxynucleotides generates 5-methylcytosine (m(5)dC), a well-established epigenetic mark. However, in higher eukaryotes much less is known about modifications affecting other deoxynucleotides. Here, we report the detection of N(6)-methyldeoxyadenosine (m(6)dA) in vertebrate DNA, specifically in Xenopus laevis but also in other species including mouse and human. Our methylome analysis reveals that m(6)dA is widely distributed across the eukaryotic genome and is present in different cell types but is commonly depleted from gene exons. Thus, direct DNA modifications might be more widespread than previously thought. 

Retracted: No

PubPeer comments:
 Authors should check another recent well executed study showing that previous reports of 6mA in higher organisms are artifactual: No evidence for DNA N6-methyladenine in mammals https: advances.sciencemag.org content 6 12 eaay3335 ,
Nebulized Anti‚ÄìIL-13 Monoclonal Antibody Fab‚Ä?Fragment Reduces Allergen-Induced Asthma
Authors: Jonathan Hacha
Jean-Michel Foidart
Maud Gueders
Kate Tomlinson
Didier D Cataldo
Natacha Rocks
Agn√®s Noel
Roger Palframan
Genevi√®ve Paulissen
Ludovic Maertens
Journal: American Journal of Respiratory Cell and Molecular Biology (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: IL-13; T helper type 2 cytokine; asthma; allergen-induced airway inflammation; hyperresponsiveness
Affiliations: Laboratory of Tumors and Developmental Biology and Department of Respiratory Diseases, Groupe Interdisciplinaire de G√©noprot√©omique Appliqu√©e (GIGA)-Research (GIGA-I¬≥ and GIGA-Cancer), University of Liege and Centre Hospitalier Universitaire, Liege (Sart-Tilman), Belgium.

Abstract:  IL-13 is a prototypic T helper type 2 cytokine and a central mediator of the complex cascade of events leading to asthmatic phenotype. Indeed, IL-13 plays key roles in IgE synthesis, bronchial hyperresponsiveness, mucus hypersecretion, subepithelial fibrosis, and eosinophil infiltration. We assessed the potential efficacy of inhaled anti-IL-13 monoclonal antibody Fab' fragment on allergen-induced airway inflammation, hyperresponsiveness, and remodeling in an experimental model of allergic asthma. Anti-IL-13 Fab' was administered to mice as a liquid aerosol generated by inExpose inhalation system in a tower allowing a nose-only exposure. BALB/c mice were treated by PBS, anti-IL-13 Fab', or A33 Fab' fragment and subjected to ovalbumin exposure for 1 and 5 weeks (short-term and long-term protocols). Our data demonstrate a significant antiasthma effect after nebulization of anti-IL-13 Fab' in a model of asthma driven by allergen exposure as compared with saline and nonimmune Fab fragments. In short- and long-term protocols, administration of the anti-IL-13 Fab' by inhalation significantly decreased bronchial responsiveness to methacholine, bronchoalveolar lavage fluid eosinophilia, inflammatory cell infiltration in lung tissue, and many features of airway remodeling. Levels of proinflammatory mediators and matrix metalloprotease were significantly lower in lung parenchyma of mice treated with anti-IL-13 Fab'. These data demonstrate that an inhaled anti-IL-13 Fab' significantly reduces airway inflammation, hyperresponsiveness, and remodeling. Specific neutralization of IL-13 in the lungs using an inhaled anti-IL-13 Fab' could represent a novel and effective therapy for the treatment of asthma. 

Retracted: No

PubPeer comments:
 maybe the author could check Fig 3?  ,
LACTB, a novel epigenetic silenced tumor suppressor, inhibits colorectal cancer progression by attenuating MDM2-mediated p53 ubiquitination and degradation
Authors: Shukui Wang
Tao Xu
Xiangxiang Liu
Huiling Sun
Xiuxiu Hu
Kaixuan Zeng
Yuqin Pan
Xiaoxiang Chen
Bangshun He
Journal: Oncogene (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Colorectal cancer; tumor suppressor; LACTB; promoter methylation; histone deacetylation
Affiliations: School of Medicine, Southeast University, Nanjing, 210009, China., General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China., School of Medicine, Southeast University, Nanjing, 210009, China. ., General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China. .

Abstract:  Colorectal cancer (CRC) is one of the most common aggressive malignancies. Like other solid tumors, inactivation of tumor suppressor genes and activation of oncogenes occur during CRC development and progression. Recently, a novel tumor suppressor, LACTB, was proposed to inhibit tumor progression, but the functional and clinical significance of this tumor suppressor in CRC remains unexplored. Herein, we found LACTB was significantly downregulated in CRC due to promoter methylation and histone deacetylation, which was associated with metastasis and advanced clinical stage. CRC patients with low LACTB expression had poorer overall survival and LACTB also determined to be an independent prognostic factor for poorer outcome. Ectopic expression of LACTB suppressed CRC cells proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and inhibited CRC growth and metastasis in vivo, while knockout of LACTB by CRISPR/Cas9 gene editing technique resulted in an opposite phenotype. Interestingly, LACTB could exert antitumorigenic effect only in HCT116 and HCT8 cells harboring wild-type TP53, but not in HT29 and SW480 cells harboring mutant TP53 or HCT116 p53-/- cells. Mechanistic studies demonstrated that LACTB could directly bind to the C terminus of p53 to inhibit p53 degradation by preventing MDM2 from interacting with p53. Moreover, ablation of p53 attenuated the antitumorigenic effects of LACTB overexpression in CRC. Collectively, our findings successfully demonstrate for the first time that LACTB is a novel epigenetic silenced tumor suppressor through modulating the stability of p53, supporting the pursuit of LACTB as a potential therapeutic target for CRC. 

Retracted: No

PubPeer comments:
 Images in Figure 3g and 4g appear to overlap after rotation. ***   ,