PReD-Bench/PRed-Bench huggingface dataset:
miR‚Ä?01b and NR3C2 co‚Äêregulate cells malignant properties and have the potential to be independent prognostic factors in breast cancer
Authors: Hongbiao Yang
Jun Ni
Changyong Wen
Meiling Wen
Xun Xi
Juntao Li
Yun Peng
Journal: Journal of Biochemical and Molecular Toxicology (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: aggressiveness; growth; independent predictor; rescue; tumor.
Affiliations: Department of Breast and Thyroid Surgery, People's Hospital of Ganzhou City, Ganzhou, China., Department of Anesthesiology, People's Hospital of Ganzhou City, Ganzhou, China., Ganzhou Inteligent Industry Innovation Research Institute, Ganzhou, China.

Abstract:  This study intends to address the function of miR-301b/nuclear receptor subfamily 3 group C member 2 (NR3C2) in breast cancer. The Cancer Genome Atlas database was processed to investigate the expression of miR-301b/NR3C2 in breast cancer samples, as well as the relationship between their expression and the prognosis of the patients. Cox regression analysis was performed to determine whether miR-301b/NR3C2 was an independent predictor of the patient's prognosis. Associations between miR-301b and NR3C2 were analyzed by prediction website, dual-luciferase assay, and Pearson correlation coefficient. Quantitative polymerase chain reaction and Western blot analyses were implemented to detect gene expression. The relevant biological characteristics of MCF7 and BCAP-37 cells were tested by cell counting kit-8, colony formation, and transwell assays. Lower expression of NR3C2, which was closely related to the bad prognosis of breast cancer patients, was presented in breast cancer samples and can be used as an independent predictor. miR-301b, as an upstream regulator of NR3C2, was highly expressed in breast cancer samples and can be used as an independent predictor as well. Notably, a higher level of miR-301b and lower level of NR3C2 were related to the reduced overall survival in patients with breast cancer. The proliferative and migratory behaviors of cells were elevated or blocked after overexpression of miR-301b or NR3C2, respectively. However, the above situation was attenuated after together upregulation of miR-301b and NR3C2. The present data afforded evidence that miR-301b may be a tumor-promoting miRNA in breast cancer, and that miR-301b/NR3C2 axis mediated tumor development from cell proliferation and migration. 

Retracted: No

PubPeer comments:
 This paper makes use of  Human breast cancer cell lines MCF7 and BCAPu201037 . Unfortunatly BCaP-37 is not a breast cancer cell line but an HeLa contaminated one. This probably explains contradictory results such as  As miRu2010301b was lower expressed in MCF7 cells and highly expressed in BCAPu201037 cells, we selected a mimic to treat MCF7 cells and an inhibitor to treat BCAPu201037 cells, which could better explain the experimental results . In any cases the conclusions of the paper in the context of breast cancer are invalidated by using both a bona fide breast cancer cell line (MCF-7) and an endocervical cell line (BcAP-37 = HeLa). See the relevant [Cellosaurus entry] ,
Estrogen receptor Œ≤ inhibits estradiol-induced proliferation and migration of MCF-7 cells through regulation of mitofusin 2
Authors: Cuizhi Geng
Li Ma
Yueping Liu
Xiaowei Qi
Jun Jiang
Journal: International journal of oncology (2013)
Discipline: CLINICAL MEDICINE
Keywords: estrogen receptor (ER) Œ≤; proliferation; migration; mitofusin 2 (mfn2); breast cancer
Affiliations: Breast Disease Center, Southwest Hospital, Third Military Medical University, Chongqing, P.R. China.

Abstract:  In the present study, we investigated whether estrogen receptor (ER) Œ≤ affected the proliferation and migration of the human breast cancer cell line MCF-7 through regulation of mitofusin 2 (mfn2). A previous study reported that mfn2 may be regulated by ER through a non-classical pathway; in this pathway, the ER modulates the activities of other transcription factors by stabilizing their binding to DNA and/or recruiting coactivators to the complex. However, the previous study, unlike the study presented here, did not directly explore the interactions between ER and mfn2. Here, RT-PCR and western blot analysis were used to test the expression of mfn2 in MCF-7 cells after exposure to different doses of estradiol (E2). The ability of cells to proliferate and migrate was determined by MTT assay and a monolayer-wounding protocol, respectively. Finally, changes in MCF-7 cell biology after transfection with ERŒ≤ or mfn2 expression vectors were investigated, and the role of ERŒ≤ in mfn2 expression was also explored. Our results showed that E2 attenuated mfn2 expression in a dose-dependent manner, concomitant with the activation of proliferation and migration of MCF-7 cells. The mfn2 expression vector effectively suppressed E2-induced upregulation of PCNA and migration in MCF-7 cells. ERŒ≤ inhibited the E2-induced mfn2 downregulation that accompanied the inhibition of proliferation and migration in MCF-7 cells. Briefly, ERŒ≤ may inhibit E2-induced proliferation and migration of MCF-7 cells through regulation of mfn2. 

Retracted: No

PubPeer comments:
 Figure 2A. * Blue boxes: The  control and  10-8 mol l panels appear to show an area of overlap. One of the panels appears rotated and stretched differently than the other.  This issue has been addressed by a 2016  Erratum which has not been indexed in PubMed. The Erratum reads:  in comparing the u2018Controlu2019 and the u201810u22128 mol lu2019 panels, the data for the u2018Controlu2019 panel had erroneously been included as the u201810u22128 mol lu2019 panel, albeit the latter panel appeared in a slightly reorientated position and was stretched longitudinally. After having re-examined our original data, we realize that the inclusion of the identical data for the u201810u22128 mol lu2019 panel was incorrect. ,
Loss of caspase-2-dependent apoptosis induces autophagy after mitochondrial oxidative stress in primary cultures of young adult cortical neurons
Authors: William W Morgan
Brian Herman
Meenakshi Tiwari
Marisa Lopez-Cruzan
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Mitochondrial dysfunction; Neuronal apoptosis; Caspase-2; Rotenone; Primary neurons
Affiliations: Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas 78229, USA.

Abstract:  Mitochondrial dysfunctions have been associated with neuronal apoptosis and are characteristic of neurodegenerative conditions. Caspases play a central role in apoptosis; however, their involvement in mitochondrial dysfunction-induced neuronal apoptosis remains elusive. In the present report using rotenone, a complex I inhibitor that causes mitochondrial dysfunction, we determined the initiator caspase and its role in cell death in primary cultures of cortical neurons from young adult mice (1-2 months old). By pretreating the cells with a cell-permeable, biotinylated pan-caspase inhibitor that irreversibly binds to and traps the active caspase, we identified caspase-2 as an initiator caspase activated in rotenone-treated primary neurons. Loss of caspase-2 inhibited rotenone-induced apoptosis; however, these neurons underwent a delayed cell death by necrosis. We further found that caspase-2 acts upstream of mitochondria to mediate rotenone-induced apoptosis in neurons. The loss of caspase-2 significantly inhibited rotenone-induced activation of Bid and Bax and the release of cytochrome c and apoptosis inducing factor from mitochondria. Rotenone-induced downstream activation of caspase-3 and caspase-9 were also inhibited in the neurons lacking caspase-2. Autophagy was enhanced in caspase-2 knock-out neurons after rotenone treatment, and this response was important in prolonging neuronal survival. In summary, the present study identifies a novel function of caspase-2 in mitochondrial oxidative stress-induced apoptosis in neurons cultured from young adult mice. 

Retracted: No

PubPeer comments:
 Figure 3A. Much more similar than exepected.  , 
 Figure 3A continued. Much more similar than expected.  ,
A zymographic study of metalloprotease activities in extracts and extracellular secretions of Leishmania (Viannia) braziliensis strains
Authors: P Cuervo
J B DE Jesus
L Sab√≥ia-Vahia
E Cupolillo
O Fernandes
F Costa Silva-Filho
Journal: Parasitology (2005)
Discipline: MICROBIOLOGY
Keywords: Leishmania (Viannia) braziliensis; proteolytic activities; metalloproteases; zymographic assays; clinical manifestations
Affiliations: Departamento de Medicina Tropical, Instituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro, Brasil.

Abstract:  Proteolytic activities of 5 strains of Leishmania (Viannia) braziliensis isolated from Brazilian and Colombian patients, presenting distinct clinical manifestations, were characterized and compared using whole-promastigote extracts and extracellular secretions. Zymographic assays concerning whole-cell extracts and supernatants resulted in the detection of high molecular weight bands, ranging from 50 to 125 kDa. Proteolytic activities from both whole-cell extracts and supernatants were optimal in a pH range 5.5 to 9.0 for all analysed strains. Such protease activities were inhibited when 10 mM 1,10-phenanthroline was assayed, strongly suggesting that the enzymes responsible for hydrolysis of the substrate belong to the metalloproteases class. Distinct profiles of metalloproteases were observed among the studied L. (V.) braziliensis strains. Differences among the microorganisms might be related to the geographical origin of the strains and/or to the clinical presentation. 

Retracted: No

PubPeer comments:
 Figure 1 - image made lighter to bring out details * Red boxes: In the pH 3.5 row, panels A (extracts at 4h) and B (supernatants at 48h) appear to show the same gel, albeit at a different exposure.  , 
 Figure 5: * Blue boxes: In left (A) panel, lanes 1407 C (Cutaneous) and IOL-L 2481 (Cutaneous) look much more similar than expected.  , 
 It is expected that the figures highlighted in red (figure 1) are similar because it is a comparison of the total extract of the parasites with their respective secretion products, at the same pH. However, the figures are not identical, only similar. This can be detected in the image as a whole, observing, for example, the blemishes and imperfections of the figure itself. See for example that in the enlarged figure B, the profile of 1407C has spots below the proteolysis band that are not observed in the total extract shown in figure A. Still in this comparison, the proteolytic band of A has a different morphology from that observed in B. Such characteristics are not due to the mere difference in image exposure. About figure 5, although the protein profile is very similar, the slots highlighted in blue present several different regions. Please see for example the main band between 92 and 52.9 kDa, the band immediately below 52.9, and the strong band immediately above 21.5 kDa. Those bands are different, so those slots are different. However, as this is an old article, we have not yet located the original images. They were generated between 2003-2004 when we were working on this paper. As soon as we have this information, we will return with more details. ,
Treprostinil inhibits proliferation and extracellular matrix deposition by fibroblasts through cAMP activation
Authors: Gabriella Murak√∂zy
Walter Klepetko
Michael Tamm
Christopher Lambers
Feng Zhao
Michael Roth
Bahil Ghanim
Peter Jaksch
Journal: Scientific Reports (2018)
Discipline: Multidisciplinary
Keywords: Idiopathic pulmonary fibrosis; ECM deposition; TGF-Œ≤1; PDGF-BB; Treprostinil
Affiliations: Department of Thoracic Surgery, Lung Transplantation Program, Medical University Vienna, W√§hringer G√ºrtel 18-20, A-1090, Vienna, Austria. ., Pulmonary Cell Research & Pneumology, Department Biomedicine, University & University Hospital Basel, Petersgraben 4, CH-4031, Basel, Switzerland., Department of Thoracic Surgery, Lung Transplantation Program, Medical University Vienna, W√§hringer G√ºrtel 18-20, A-1090, Vienna, Austria., Fourth Military Medical University, Xi'an, P. R. China.

Abstract:  Idiopathic pulmonary fibrosis (IPF) is characterized by peripheral lung fibrosis and increased interstitial extracellular matrix (ECM) deposition. In IPF, tumor growth factor (TGF)-Œ≤1 which is the major stimulus of ECM deposition, and platelet derived growth factor (PDGF)-BB is a potent stimulus of fibrosis. Thus, the effect of Treprostinil on TGF-√ü1 and PDGF-induced fibroblast proliferation and ECM deposition was investigated. Human peripheral lung fibroblasts of seven IPF patients and five lung donors were stimulated by PDGF, or TGF-Œ≤1, or the combination. Cells were pre-incubated (30 min) with either Treprostinil, forskolin, di-deoxyadenosine (DDA), or vehicle. Treprostinil time dependently activated cAMP thereby preventing PDGF-BB induced proliferation and TGF-Œ≤1 secretion. Cell counts indicated proliferation; Œ±-smooth muscle actin (Œ±-SMA) indicted differentiation, and collagen type-1 or fibronectin deposition remodeling. Myo-fibroblast indicating Œ±-SMA expression was significantly reduced and its formation was altered by Treprostinil. Collagen type-I and fibronectin deposition were also reduced by Treprostinil. The effect of Treprostinil on collagen type-I deposition was cAMP sensitive as it was counteracted by DDA, while the effect on fibronectin was not cAMP mediated. Treprostinil antagonized the pro-fibrotic effects of both PDGF-BB and TGF-Œ≤1 in primary human lung fibroblasts. The data presented propose a therapeutic relevant anti-fibrotic effect of Treprostinil in IPF. 

Retracted: No

PubPeer comments:
 Figure 5 appears to have a repeated image. Could the authors please check? ***  , 
 #1 We became aware of this duplication shortly after the publication went online and have submitted a request for an erratum. The journal acknowledged the request of the erryatum, but did not yet send us their decission. ,
Clusterin is a potential molecular predictor for ovarian cancer patient's survival: targeting clusterin improves response to paclitaxel
Authors: Takashi Mitamura
Masayoshi Hosaka
Lei Wang
Mohamed K Hassan
Shinya Tanaka
Yimin Han
Hidemichi Watari
Noriaki Sakuragi
Journal: Journal of Experimental & Clinical Cancer Research (2011)
Discipline: CLINICAL MEDICINE
Keywords: Clusterin; ovarian cancer; antiapoptotic; predictor molecule; survival
Affiliations: Department of Obstetrics and Gynecology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Abstract:  Background: Clusterin is a cytoprotective chaperone protein involved in numerous physiological processes, carcinogenesis, tumor growth and tissue remodelling. The purpose of this study was to investigate whether clusterin (CLU), an antiapoptotic molecule, could be a potential predictor molecule for ovarian cancer and whether or not targeting this molecule can improve survival of ovarian cancer patients. Methods: Clusterin expression was compared between ten primary and their recurrent tumors from same patients immunohistochemically. We analyzed prognostic significance of CLU expression in another 47 ovarian cancer tissue samples by immunohistochemistry. We used small interference RNA to knock down CLU in the chemo-resistant ovarian cancer cell lines. KF-TX and SKOV-3-TX, paclitaxel-resistant ovarian cancer cells, were established from parental KF and SKOV-3 chemo-sensitive cell lines, respectively. Either siRNA or second generation antisense oligodeoxynucleotide against CLU (OGX-011), which is currently evaluated in clinical phase II trials in other cancer s, was used to modulate sensitivity to paclitaxel (TX) in ovarian cancer cells in vitro. Cellular viability assay, FACS analysis and annexin V staining were used to evaluate the comparative effect of CLU knocking down in ovarian cancer cells. Results: Immunohistochemical analysis of CLU expression in primary ovarian cancer tissue specimens and their recurrent counterparts from same patients demonstrated higher expression of CLU in the recurrent resistant tumors compared with their primary tumors. High expression of CLU by immunohistochemistry among 47 surgical tissue specimens of early-stage (stage I/II) ovarian cancer, who underwent complete cytoreduction as a primary surgery, significantly related to poor survival, while none of other clinicopathological factors analyzed were related to survival in this patient cohort. Secretory CLU (s-CLU; 60 KDa) expression was upregulated in TX-resistant ovarian cancer cells compared to parental cells. Transfection of siRNA or OGX-011 clearly reduced CLU expression. Cell viability assay, FACS analysis and annexin V staining demonstrated that targeting CLU expression by siRNA or OGX-011 sensitized ovarian cancer cells to TX. Conclusion: We conclude that CLU could be a potential molecular target to predict survival while targeting this s-CLU may improve survival of patients with ovarian cancer. 

Retracted: No

PubPeer comments:
 Figure 3. * Blue boxes. The Ponceau S panel representing KF cells appears to show an overlap with the panel representing the KF-TX cells.  ,
An RNA code for the FOX2 splicing regulator revealed by mapping RNA-protein interactions in stem cells
Authors: Gene W Yeo
Nicole G Coufal
Xiang-Dong Fu
Tiffany Y Liang
Fred H Gage
Grace E Peng
Journal: Nature Structural & Molecular Biology (2009)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: regulated splicing; post-transcriptional gene expression; RNA elements; splicing regulator; FOX2
Affiliations: Crick-Jacobs Center for Theoretical and Computational Biology, Salk Institute, 10010 North Torrey Pines Road, La Jolla, California 92037, USA. 

Abstract:  The elucidation of a code for regulated splicing has been a long-standing goal in understanding the control of post-transcriptional gene expression events that are crucial for cell survival, differentiation and development. We decoded functional RNA elements in vivo by constructing an RNA map for the cell type-specific splicing regulator FOX2 (also known as RBM9) via cross-linking immunoprecipitation coupled with high-throughput sequencing (CLIP-seq) in human embryonic stem cells. The map identified a large cohort of specific FOX2 targets, many of which are themselves splicing regulators, and comparison between the FOX2 binding profile and validated splicing events revealed a general rule for FOX2-regulated exon inclusion or skipping in a position-dependent manner. These findings suggest that FOX2 functions as a critical regulator of a splicing network, and we further show that FOX2 is important for the survival of human embryonic stem cells. 

Retracted: No

PubPeer comments:
 Above: Fig 3 (C) and (D)  Transwell analysis showed miR-675 overexpression promoted invasion and migration of U251MG cells . Below: Fig 4 (C) and (D)  Transwell analysis showed the decreased expression of miR-675 inhibited invasion and migration of U251MG cells .  Flipped horizontally, the NC Mimics panel of 3D matches the miR-675-inhibitor panel of 4C; except where they don t match. Flipped vertically, the miR-675-mimics panel of 3D matches the miR-675-inhibitor panel of 4D; except where they don t match. This does not inspire faith in the veridicality of these results. ,
MiR-143 targets CTGF and exerts tumor-suppressing functions in epithelial ovarian cancer
Authors: Jin He
Na Li
Hongmei Xu
Longjie Xu
Lufei Wang
Journal: American journal of translational research (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: CTGF; epithelial ovarian carcinoma; miR-143; microRNAs.
Affiliations: Department of Ophthalmology, The Second Hospital of Jilin University Changchun 130041, Jilin Province, P.R. China., Department of Obstetrics and Gynecology, The First Hospital of Jilin University Changchun 130021, Jilin Province, P.R. China.

Abstract:  A series of recent studies suggested that miR-143 might involve in the tumorigenesis and metastasis of various cancer types. However, the biological function and underlying mechanisms of miR-143 in human epithelial ovarian carcinoma (EOC) remain unknown. Therefore, this study aimed to investigate the miR-143 expression and its clinical diagnosis significance in patients suffering EOC and to analyze its role and underlying molecular mechanism in EOC. Our result showed that the expression levels of miR-143 were downregulated in EOC tissues and cell lines, was associated with International Federation of Gynaecology and Obstetrics (FIGO) stage, pathological grade and lymph node metastasis (all P &lt; 0.01) . Overexpression of miR-143 significantly inhibited EOC cell proliferation, migration, and invasion. Furthermore, computational algorithm combined with luciferase reporter assays identified connective tissue growth factor (CTGF) as the direct target of miR-143 in EOC cells. The expression level of CTGF was significantly increased in EOC tissues, was inversely correlated with miR-143 expression in clinical EOC tissues. Knockdown of CTGF mimicked the suppression effect induced by miR-143 overexpression. Restoration of CTGF expression partially reversed the suppression effect induced by miR-143 overexpression. These results suggested that miR-143 inhibited EOC cell proliferation, migration, and invasion, at least in part, via suppressing CTGF expression. 

Retracted: No

PubPeer comments:
 Fig 2C.  , 
 Corrected [15 July 2021] . -------------------------- In this paper, a mistake has been found in Figure 2C. The image for 0 hour of miR-NC group was inadvertently presented with the same image for 0 hour of miR-143 treatment. We have accordingly replaced the Figure 2C with the corrected image. The corrected Figure 2 is enclosed. Change in representative image does not affect the interpretation of our data. The figure legend is correct as published and is also shown below for reference. The error has no bearings on the interpretation of the results, nor do they influence the conclusions of the work.  ,
Restoring the Sense of Touch Using a Sensorimotor Demultiplexing Neural Interface
Authors: Patrick D Ganzer
David A Friedenberg
Doug J Weber
Michael A Schwemmer
Samuel C Colachis 4th
Marcia A Bockbrader
Gaurav Sharma
Collin F Dunlap
Carly E Swiftney
Adam F Jacobowitz
Journal: Cell (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: brain-computer interface; cortex; decoding; demultiplex; machine learning
Affiliations: Medical Devices and Neuromodulation, Battelle Memorial Institute, 505 King Avenue, Columbus, OH 43201, USA. Electronic address: ., Medical Devices and Neuromodulation, Battelle Memorial Institute, 505 King Avenue, Columbus, OH 43201, USA., Advanced Analytics and Health Research, Battelle Memorial Institute, 505 King Avenue, Columbus, OH 43201, USA., Medical Devices and Neuromodulation, Battelle Memorial Institute, 505 King Avenue, Columbus, OH 43201, USA; Department of Physical Medicine and Rehabilitation, The Ohio State University, Columbus, OH 43210, USA., Medical Devices and Neuromodulation, Battelle Memorial Institute, 505 King Avenue, Columbus, OH 43201, USA; Department of Bioengineering, University of Pittsburgh, 4200 Fifth Avenue, Pittsburgh, PA 15260, USA., Department of Physical Medicine and Rehabilitation, The Ohio State University, Columbus, OH 43210, USA.

Abstract:  Paralyzed muscles can be reanimated following spinal cord injury (SCI) using a brain-computer interface (BCI) to enhance motor function alone. Importantly, the sense of touch is a key component of motor function. Here, we demonstrate that a human participant with a clinically complete SCI can use a BCI to simultaneously reanimate both motor function and the sense of touch, leveraging residual touch signaling from his own hand. In the primary motor cortex (M1), residual subperceptual hand touch signals are simultaneously demultiplexed from ongoing efferent motor intention, enabling intracortically controlled closed-loop sensory feedback. Using the closed-loop demultiplexing BCI almost fully restored the ability to detect object touch and significantly improved several sensorimotor functions. Afferent grip-intensity levels are also decoded from M1, enabling grip reanimation regulated by touch signaling. These results demonstrate that subperceptual neural signals can be decoded from the cortex and transformed into conscious perception, significantly augmenting function. 

Retracted: No

PubPeer comments:
 Several Western immunoblots in Figure 3 share the same background. LC3I and II have similar molecular weight (16-18 and 14-16 kDa, respectively) and should be presented together.  ,
Selective targeting of checkpoint kinase 1 in tumor cells with a novel potent oncolytic adenovirus
Authors: Fei Ye
Ding Ma
Qinglei Gao
Yunping Lu
Gang Xu
Xiaoyuan Huang
Shxuan Wang
Gang Chen
Kanyan Li
Jianfeng Zhou
Mei Huang
Liang Zhuang
Journal: Molecular Therapy (2006)
Discipline: CLINICAL MEDICINE
Keywords: Retraction; Similarities; Image analysis; Image recycling; Data reuse
Affiliations: Cancer Biology Research Center, TongJi Hospital, TongJi Medical School, Huazhong University of Science & Technology, WuHan, Hubei 430030, People's Republic of China.

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the editor-in-chief. Similarities were reported between images in this article and an article in Clinical Cancer Research (Zhou et al., 2005, Clin. Cancer Res. 11, 8431-8440, https://10.1158/1078-0432.CCR-05-1085). Q.J., J.Z., X.H., G.C., Y.L., K.L., L.Z., and D.M. were all authors of the Clinical Cancer Research paper as well. These concerns were initially reported in a Pubpeer thread (https://pubpeer.com/publications/FF881782FF5AFD316D42E0C0F00766). Image analysis performed by the editorial office confirmed findings of image recycling in Figures 2A and 3B of the Molecular Therapy article. This reuse (and in part misrepresentation) of data without appropriate attribution represents a severe abuse of the scientific publishing system. 

Retracted: No

PubPeer comments:
 In Fig.2A, the first two panels of  Hela cells and  MCF-7 cells appear to look more similar than expected. Marked in red box.  , 
 The two panel shown in Figure 2A appears to look similar. Marked in blue box Note the different treatments.  , 
 Fig. 5B in this paper and Fig. 4C in another paper by the same group (doi:10.1158 1078-0432.CCR-05-1085). More similar than expected.  , 
 The image of one plate in Fig. 2A was reused, after rotation, in Fig. 2A in another paper (doi:10.1158 1078-0432.CCR-05-1085) by the same author group, which represent different treatments.  , 
 The actin band in Fig. 3A was cropped and reused from that in Fig. 3A in another paper (doi: 10.1007 s10495-006-9421-4) by the same author group. , 
  , 
 Retracted [28 December 2022] . This thread is cited.  This article has been retracted at the request of the editor-in-chief. Similarities were reported between images in this article and an article in Clinical Cancer Research (Zhou et al., 2005, Clin. Cancer Res. 11, 8431-8440, https: 10.1158 1078-0432.CCR-05-1085). Q.J., J.Z., X.H., G.C., Y.L., K.L., L.Z., and D.M. were all authors of the Clinical Cancer Research paper as well. These concerns were initially reported in a Pubpeer thread . Image analysis performed by the editorial office confirmed findings of image recycling in Figures 2A and 3B of the Molecular Therapy article. This reuse (and in part misrepresentation) of data without appropriate attribution represents a severe abuse of the scientific publishing system. ,
<p>MicroRNA-802 Inhibits Cell Proliferation and Induces Apoptosis in Human Laryngeal Cancer by Targeting cAMP-Regulated Phosphoprotein 19</p>
Authors: Huafu Ye
Xiaoqiong Wang
Qiaozhi Jin
Yong Li
Journal: Cancer Management and Research (2020)
Discipline: CLINICAL MEDICINE
Keywords: ARPP19; cell cycle; laryngeal carcinoma; miR-802; proliferation.
Affiliations: E.N.T. Department, Taizhou Municipal Hospital, Taizhou City, Zhejiang Province 318000, People's Republic of China.

Abstract:  Background/aims: miR-802 plays a key role in cancer progression and development. The purpose of this work is to investigate the functional role of miR-802 in laryngeal cancer and to elucidate the function of miR-802 and cAMP-regulated phosphoprotein 19 (ARPP19) on laryngeal cancer. Methods: RT-qPCR was applied to study the expression level of ARPP19 and miR-802 in the laryngeal carcinoma cell lines and tissues. CCK-8, colony formation, flow cytometry (FACS) assay were used to study the effect of ARPP19 and miR-802 on apoptosis, proliferation, and cell cycle of laryngeal carcinoma cells. Target gene prediction and luciferase reporter gene assay were applied to identify target gene of miR-802. The transcriptional mRNA and protein expression levels of ARPP19 were measured by RT-qPCR or Western blotting. Results: miR-802 was down-regulated in laryngeal carcinoma cell lines and tissues. Laryngeal cancer cells transfected by miR-802 mimic were significantly inhibited in the terms of cell colony formation and proliferation. Furthermore, miR-802 can inhibit the expression level of ARPP19 by directly targeting the 3' untranslated region (3'-UTR) of ARPP19. Overexpression of the ARPP19 gene can reverse the suppressive effect of miR-802 on laryngeal cancer cells. Conclusion: miR-802 can exert tumor suppressor effects in laryngeal carcinoma by targeting ARPP19, indicating that miR-802 protein may play a role of potential therapeutic target for clinical laryngeal cancer. 

Retracted: Yes

PubPeer comments:
  All authors agree to retract the above article. After intense investigations, Dennis Rottlaender has admitted to committing intentional and systematic manipulation of the electrophysiological data in Figures 2, A and D, 3A, 4B, 5, A and D, and 6, A and D. Dr. Rottlaender acted alone, and the other authors were not previously aware of these manipulations. All authors deeply regret the impact of this action. ,
Regulation of the deubiquitinating enzyme CYLD by IkappaB kinase gamma-dependent phosphorylation
Authors: Minying Zhang
Erica Granger
Shao-Cong Sun
William Reiley
Xuefeng Wu
Journal: Molecular and Cellular Biology (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Tumor suppressor; CYLD; deubiquitinating enzyme; DUB; ubiquitination
Affiliations: Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, 500 University Dr., Hershey, PA 17033, USA.

Abstract:  Tumor suppressor CYLD is a deubiquitinating enzyme (DUB) that inhibits the ubiquitination of key signaling molecules, including tumor necrosis factor (TNF) receptor-associated factor 2 (TRAF2). However, how the function of CYLD is regulated remains unknown. Here we provide evidence that inducible phosphorylation of CYLD is an important mechanism of its regulation. Under normal conditions, CYLD dominantly suppresses the ubiquitination of TRAF2. In response to cellular stimuli, CYLD undergoes rapid and transient phosphorylation, which is required for signal-induced TRAF2 ubiquitination and activation of downstream signaling events. Interestingly, the CYLD phosphorylation requires IkappaB kinase gamma (IKKgamma) and can be induced by IKK catalytic subunits. These findings suggest that CYLD serves as a novel target of IKK and that the site-specific phosphorylation of CYLD regulates its signaling function. 

Retracted: No

PubPeer comments:
 Figure 2A. Much more similar than expected. https: imgur.com HrYbj00 ,
Glutaminyl cyclase-mediated toxicity of pyroglutamate-beta amyloid induces striatal neurodegeneration
Authors: Hans-Ulrich Demuth
Stephan von H√∂rsten
Fabio Canneva
Stephanie Kohlmann
Christoph B√§uscher
Sigrid Graubner
Holger Cynis
Wolfgang Jagla
Anca Alexandru
Stephan Schilling
Reinhard Sedlmeier
Andreas Becker
Journal: BMC Neuroscience (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Posttranslational modifications; beta amyloid; N-terminal pyroglutamate; enzymatic glutaminyl cyclase; pE3-AŒ≤
Affiliations: Department of Experimental Therapy, Friedrich-Alexander-University Erlangen-N√ºrnberg, Palmsanlage 5, 91054 Erlangen, Germany. .

Abstract:  Background: Posttranslational modifications of beta amyloid (AŒ≤) have been shown to affect its biophysical and neurophysiological properties. One of these modifications is N-terminal pyroglutamate (pE) formation. Enzymatic glutaminyl cyclase (QC) activity catalyzes cyclization of truncated AŒ≤(3-x), generating pE3-AŒ≤. Compared to unmodified AŒ≤, pE3-AŒ≤ is more hydrophobic and neurotoxic. In addition, it accelerates aggregation of other AŒ≤ species. To directly investigate pE3-AŒ≤ formation and toxicity in vivo, transgenic (tg) ETNA (E at the truncated N-terminus of AŒ≤) mice expressing truncated human AŒ≤(3-42) were generated and comprehensively characterized. To further investigate the role of QC in pE3-AŒ≤ formation in vivo, ETNA mice were intercrossed with tg mice overexpressing human QC (hQC) to generate double tg ETNA-hQC mice. Results: Expression of truncated AŒ≤(3-42) was detected mainly in the lateral striatum of ETNA mice, leading to progressive accumulation of pE3-AŒ≤. This ultimately resulted in astrocytosis, loss of DARPP-32 immunoreactivity, and neuronal loss at the sites of pE3-AŒ≤ formation. Neuropathology in ETNA mice was associated with behavioral alterations. In particular, hyperactivity and impaired acoustic sensorimotor gating were detected. Double tg ETNA-hQC mice showed similar AŒ≤ levels and expression sites, while pE3-AŒ≤ were significantly increased, entailing increased astrocytosis and neuronal loss. Conclusions: ETNA and ETNA-hQC mice represent novel mouse models for QC-mediated toxicity of truncated and pE-modified AŒ≤. Due to their significant striatal neurodegeneration these mice can also be used for analysis of striatal regulation of basal locomotor activity and sensorimotor gating, and possibly for DARPP-32-dependent neurophysiology and neuropathology. The spatio-temporal correlation of pE3-AŒ≤ and neuropathology strongly argues for an important role of this AŒ≤ species in neurodegenerative processes in these models. 

Retracted: No

PubPeer comments:
 legend not clear: Fig 8 C+D (E8-hQC hom wt ) is duplicated as well as Fig 5F and 8D  Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Retracted: Down‚Äêregulation of microRNA let‚Ä?d inhibits the proliferation and invasion of trophoblast cells in preeclampsia
Authors: Yan Cai
Xu Dai
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: apoptosis; invasion; microRNA let-7d; preeclampsia; primary isolation
Affiliations: Department of Gynaecology and Obstetrics, The Fourth Hospital of Harbin Medical University, Harbin, P.R. China., Department of, Obstetrics, The Fourth Hospital of Harbin Medical University, Harbin, P.R. China.

Abstract:  Preeclampsia (PE) is a serious pregnancy complication that continues to adverse effects on mother and the fetus. The study investigated the effect of microRNA let-7d (miR-let-7d) on the proliferation and invasion of trophoblast cells (TC) in PE. In situ hybridization techniques were employed to evaluate the miR-let-7d expressions in the placental tissues from 63 PE patients as well as 65 normal placental tissues. Transfection of pre-let-7d, anti-let-7d, and their corresponding control sequences was performed in TCs obtained from PE. The blank group was composed of TCs no transfection and normal group consisted of normal TCs. Expressions of proliferation and invasion markers in TCs were detected by qRT-PCR. Proliferation, apoptosis, and the invasion ability of the TCs were determined using a CCK-8 assay, flow cytometry, and Transwell assay. In comparison to the normal placental tissues, PE placental tissues exhibited increased levels of let-7d expression. Following transfection of anti-let-7d, when compared with the blank group, the anti-let-7d group displayed increased levels of proliferation ability, expression of proliferation labeling proteins PCNA and Ki67, number of TCs as well as expressions of the invasion related proteins MMP-2, MMP-9, and TIMP-1. In contrast declines in cell apoptosis rate were observed. Compared with the blank group, the changes of the indexes were reversed in the pre-let-7d group. The study provided evidence suggesting that low expression levels of miR-let-7d plays a central role in suppressing apoptosis in addition to promoting the proliferation and invasion of PE TCs. 

Retracted: Yes

PubPeer comments:
 This paper was proven to be wrong: https: www.sciencedirect.com science article pii S2542529317302316 In fact the authors just measured the superconductivity of Sn (Tc = 3.7 K) impurities in their sample. The Sn comes from the vapour transport grown crystals. This synthesis pathway requires Sn and SnI4. That s why they see only a very small superconducting volume fraction. All the standard characterization measurements (specific heat, resistivity, elemental analysis) of the samples are missing. ,
MicroRNA-27 (miR-27) targets prohibitin and impairs adipocyte differentiation and mitochondrial function in human adipose-derived stem cells
Authors: Ting Kang
Leonard Anderson
Y Eugene Chen
Wei Xu
Wan Lu
Dong Liu
Methode Bacanamwo
Winston Thompson
Journal: Journal of Biological Chemistry (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Adipogenesis; Cell Differentiation; MicroRNA; Mitochondria; Prohibitin
Affiliations: From the Cardiovascular Research Institute.

Abstract:  Prohibitin (PHB) has been reported to play a crucial role in adipocyte differentiation and mitochondrial function. However, the regulative mechanism of PHB during adipogenesis remains unclear. In this study, we determined that the levels of both microRNA (miR)-27a and miR-27b were down-regulated following adipogenic induction of human adipose-derived stem cells, whereas the mRNA level of PHB was up-regulated. Overexpression of miR-27a or miR-27b inhibited PHB expression and adipocyte differentiation. Using PHB 3'-UTR luciferase reporter assay, we observed that miR-27a and miR-27b directly targeted PHB in human adipose-derived stem cells. A compensation of PHB partially restored the adipogenesis inhibited by miR-27. Moreover, we demonstrated the novel finding that ectopic expression of miR-27a or miR-27b impaired mitochondrial biogenesis, structure integrity, and complex I activity accompanied by excessive reactive oxygen species production. Our data suggest that miR-27 is an anti-adipogenic microRNA partly by targeting PHB and impairing mitochondrial function. Pharmacological modulation of miR-27 function may provide a new therapeutic strategy for the treatment of obesity. 

Retracted: No

PubPeer comments:
 There are two undeclared splicing sites in Fig. 4A.  , 
 Thank you Ovatella Firminii. I agree with and appreciate your comment. The journal has been contacted. , 
 2020 correction. https: www.jbc.org content 295 48 16468.short VOLUME 288 (2013) PAGES 34394u201334402 The immunoblots in Figs. 2C and 4A had undeclared splices. We have repeated the experiments, and the corrected figures contain no splices. This correction does not affect the results or conclusions of this work. In the eighth line from the last in the right column of page 34396, u201cProhibitin Targets miR-27a and miR-27b in ASCu201d should read u201cmiR-27a and miR-27b Target Prohibitin in ASC.u201d The authors sincerely apologize for any inconvenience these errors may have caused readers. ,
LncRNA SNHG16 Facilitates Nasopharyngeal Carcinoma Progression by Acting as ceRNA to Sponge miR-520a-3p and Upregulate MAPK1 Expression
Authors: Tao Wang
Yingying Zhao
Qingwei Wu
Runjie Shi
Journal: Cancer Management and Research (2021)
Discipline: CLINICAL MEDICINE
Keywords: MAPK1; ceRNA; lncRNA SNHG16; miR-520a-3p; nasopharyngeal carcinoma.
Affiliations: Department of Otorhinolaryngology Head and Neck Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.

Abstract:  Background: Accumulating evidence shows that lncRNAs are widely involved cellular processes of various tumors. The aim of this study was to explore the potential role and molecular mechanism of lncRNA SNHG16 in nasopharyngeal carcinoma (NPC). Methods: SNHG16, miR-520a-3p, and MAPK1 levels were measured by RT-qPCR assay. CCK-8, colony formation, transwell, and flow cytometry assays were adopted to analyze the proliferation, migration, invasion, and apoptosis of NPC cell lines (SUNE1 and 5-8F). Murine xenograft model was used to investigate tumor growth and metastasis in vivo. Immunohistochemical staining was employed to evaluate the levels of Bcl-2, cleaved caspase-3, Bax, and Ki-67. Dual-luciferase reporter assays were conducted to analyze the binding ability between miR-520a-3p and SNHG16 or MAPK1. Results: SNHG16 was overexpressed in NPC tissues and cells. High SNHG16 expression indicated a poor prognosis. SNHG16 knockdown could cause significant inhibition on cell proliferation and metastasis, induce cell apoptosis in NPC cells, and repressed tumor growth and metastasis in vivo. Additionally, SNHG16 could directly bind to miR-520a-3p, thus positively regulating MAPK1 expression. Moreover, functional analysis indicated that miR-520a-3p exerted a tumor-suppressing role in NPC progression. Rescue assays demonstrated that MAPK1 upregulation could abrogate the inhibitory effects on NPC cell proliferation and metastasis, as well as the promoting effects on NPC cell apoptosis caused by SNHG16 knockdown. In conclusion, SNHG16 contributed to the proliferation and metastasis of NPC cells by modulating the miR-520a-3p/MAPK1 axis. Conclusion: These results suggest that SNHG16 acts as an oncogene in the progression of NPC via modulating the miR-520a-3p/MAPK1 axis. 

Retracted: No

PubPeer comments:
 In the flow-cytometry plots in this paper, dots come in several levels of saturation - saturated red data points are interspersed with faded pink ones. Is this normal? Here, Fig 5C,  Flow cytometry assay was carried out to analyze cell apoptosis of SUNE1 and 5u20138F cells.   I used the high-resolution images [from PMC] . ,
Structure of human complement C8, a precursor to membrane attack
Authors: Rossen Donev
Susan M Lea
Pietro Roversi
B Paul Morgan
Oscar Llorca
Doryen Bubeck
Journal: Journal of Molecular Biology (2011)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Complement component C8; membrane attack complex (MAC); antibacterial; immune effector; high-resolution structures
Affiliations: University of Oxford, Wellcome Trust Centre for Human Genetics, Oxford OX3 7BN, UK.

Abstract:  Complement component C8 plays a pivotal role in the formation of the membrane attack complex (MAC), an important antibacterial immune effector. C8 initiates membrane penetration and coordinates MAC pore formation. High-resolution structures of C8 subunits have provided some insight into the function of the C8 heterotrimer; however, there is no structural information describing how the intersubunit organization facilitates MAC assembly. We have determined the structure of C8 by electron microscopy and fitted the C8Œ±-MACPF (membrane attack complex/perforin)-C8Œ≥ co-crystal structure and a homology model for C8Œ≤-MACPF into the density. Here, we demonstrate that both the C8Œ≥ protrusion and the C8Œ±-MACPF region that inserts into the membrane upon activation are accessible. 

Retracted: No

PubPeer comments:
 Figure 1b appears to have a repeated image. ***  ,
Could treatment with botulinum toxin protect against subsequent infection with COVID-19?
Authors: P J Finiels
M de Boutray
D Batifol
P Jammet
S Galmiche
Journal: Journal of Stomatology Oral and Maxillofacial Surgery (2021)
Discipline: CLINICAL MEDICINE
Keywords: Acetylcholine blocking; Botulinum toxin; COVID-19.
Affiliations: Maxillofacial Surgery Department, Montpellier University Hospital Gui de Chauliac, Montpellier, France. Electronic address: ., Department of Orthopedics, Traumatology and Spine Neurosurgery, Al√®s General Hospital, Al√®s, France., Maxillofacial Surgery Department, Montpellier University Hospital Gui de Chauliac, Montpellier, France.

Abstract:  We report comparative results, over three months, of the impact of SARS-CoV2 in our patients injected with botulinum toxin for functional purposes, compared to the general population. Botulinum neurotoxin type A (BoNT/A) is known to block acetylcholine (ACh) as well as many other neuroreceptors and neuromodulators. The recent mention of a potential protective effect of nicotine in COVID 19, by blocking ACh, attracted our attention and guided the present study. Our results show a significant difference between the number of infected individuals in the general population and the number of patients injected with BoNT/A who showed signs of COVID 19. 

Retracted: No

PubPeer comments:
 Can the authors explain why they cite Ostaszewski et al., 2020, Sci Data, as reference ([7] in the article) to the claim  The percentage of our patients infected was less than 1%, whereas, according to the Pasteur Institute, 4.4% of French people have reportedly been infected [7] ? ,
Collateral sensitivity of multidrug-resistant cells to the orphan drug tiopronin
Authors: Matthew D Hall
Misty D Handley
Kyle R Brimacombe
Andr√©s E Dulcey
Gary Griffiths
Pavitra Kannan
Andrew S Goldsborough
Michael M Gottesman
Kristen M Pluchino
Journal: Journal of medicinal chemistry (2011)
Discipline: CHEMISTRY
Keywords: cancer; multidrug resistance; tiopronin; P-glycoprotein; MRP1
Affiliations: Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States, Imaging Probe Development Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Rockville, Maryland, United States, Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States

Abstract:  A major challenge in the treatment of cancer is multidrug resistance (MDR) that develops during chemotherapy. Here we demonstrate that tiopronin (1), a thiol-substituted N-propanoylglycine derivative, was selectively toxic to a series of cell lines expressing the drug efflux pump P-glycoprotein (P-gp, ABCB1) and MRP1 (ABCC1). Treatment of MDR cells with 1 led to instability of the ABCB1 mRNA and consequently a reduction in P-gp protein, despite functional assays demonstrating that tiopronin does not interact with P-gp. Long-term exposure of P-gp-expressing cells to 1 sensitized them to doxorubicin and paclitaxel, both P-gp substrates. Treatment of MRP1-overexpressing cells with tiopronin led to a significant reduction in MRP1 protein. Synthesis and screening of analogues of tiopronin demonstrated that the thiol functional group was essential for collateral sensitivity while substitution of the amino acid backbone altered but did not destroy specificity, pointing to future development of targeted analogues. 

Retracted: Yes

PubPeer comments:
    , 
   , 
  , 
  , 
 So a smaller piece of a government large government report was published with fewer authors? I fail to see the issue here. , 
 I disagree with potato virus . This seems to be multiple uses of the same data. If this is the case it may be salami slicing or indeed self plagiarism. As a reviewer and editor myself this a concern since (at the very best) it makes an already crumbling peer review process feel more pressure. ,