PReD-Bench/PRed-Bench huggingface dataset:
Complimentary action: C1q increases ganglion cell survival in an in vitro model of retinal degeneration
Authors: Karin Arnér
Anna M Blom
Linnéa Taylor
Fredrik Ghosh
Journal: Journal of Neuroimmunology (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Adult retina; C1q; Ganglion cell; Neuroinflammation; Retinal degeneration
Affiliations: Department of Clinical Sciences, Ophthalmology, Lund University, Lund, Sweden. Electronic address: ., Department of Clinical Sciences, Ophthalmology, Lund University, Lund, Sweden., Department of Translational Medicine, Lund University, Malmö, Sweden.

Abstract:  Using a previously described retinal explant culture system as an acute injury model, we here explore the role of C1q, the initiator of the classical complement pathway, in neuronal cell survival and retinal homeostasis. Full-thickness adult rat retinal explants were divided into four groups, receiving the following supplementation: C1q (50nM), C1-inhibitor (C1-inh; Berinert; 500mg/l), C1q+C1-inh, and no supplementation (culture controls). Explants were kept for 12h or 2days after which they were examined morphologically and with a panel of immunohistochemical markers. C1q supplementation protects ganglion cells from degeneration within the explant in vitro system. This effect is correlated to an attenuated endogenous production of C1q, and a quiesced gliotic response. 

Retracted: No

PubPeer comments:
 In figure 3 (G, H) and 6 (E, F) images of tissues undergone different treatments overlap. ![file] ,
CRISPR/Cas9-mediated LMP1 knockout inhibits Epstein-Barr virus infection and nasopharyngeal carcinoma cell growth
Authors: Haifeng Huo
Guohua Hu
Journal: Infectious Agents and Cancer (2019)
Discipline: CLINICAL MEDICINE
Keywords: CRISPR/Cas9; Epstein-Barr virus (EBV); Growth; LMP1; Nasopharyngeal carcinoma.
Affiliations: Department of Otorhinolaryngology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016 China.

Abstract:  Background: A strong association between Epstein-Barr virus (EBV) infection and nasopharyngeal carcinoma (NPC) has been widely recognized in recent decades. The aim of the present study was to investigate latent membrane protein 1 (LMP1) regulation of nasopharyngeal carcinoma (NPC) CNE-2 cell growth and then examine the effects of LMP1-knockout with CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats)/Cas9on Epstein-Barr virus (EBV) infection and CNE-2 cell growth. Methods: Human NPC CNE-2 cells were infected with the recombinant LMP1- and LMP2A-carrying lentivirus, and then examined for cell growth with the colony forming assay as well as for the activation of transcription of eukaryotic translation initiation factor 4E (eIF4E) with reverse-transcriptase quantitative polymerase chain reaction (RT-qPCR) and western blot. CRISPR/Cas9-mediated knockout of LMP1 or LMP2A was performed with a single-guide RNA (sgRNA) targeting sequences within LMP1 or LMP2A. The knockout effect and the EBV proliferation were examined with RT-qPCR, western blot and cell growth assay. Results: LMP1 overexpression promoted CNE-2 cell growth, compared to LMP2A overexpression. Loss-of-function experiments confirmed that eukaryotic translation initiation factor 4E (eIF4E) upregulation mediated this effect. LMP1 knockout significantly inhibited EBV proliferation in CNE-2 cells and markedly inhibited LMP1-mediated promotion of cell growth. The knockout of either LMP1 or LMP2A blocked the eIF4E activation, which is induced either by the EBV infection or by the overexpression of LMP1 or LMP2A. Conclusion: We confirmed the LMP1-mediated promotion of NPC cell growth. Such promotion can be effectively blocked by CRISPR/Cas9-mediated LMP1 knockout. Precise LMP1 knockout might be a promising method for targeted inhibition of EBV infection and NPC cell growth. 

Retracted: No

PubPeer comments:
 Another reader brought multiple concerns about this paper to my attention. Perhaps the authors could share the original uncropped scans used to generate Figure 6C. There appear to be multiple indications of splicing. *** Inverse ![file] *** Original ![file] , 
 And out of curiosity, why did the authors repeat these two figures on adjacent pages? Not sure itu2019s inappropriate, just odd. *** ![file] , 
 Sharp features in Figure 3 suggest undisclosed splicing. u201cEditedu201d and u201cNot editedu201d labels (unironically) included in original. I acknowledge that the features in 3C may be compression artifacts. *** ![file] ,
Caspase-8-dependent HER-2 cleavage in response to tumor necrosis factor alpha stimulation is counteracted by nuclear factor kappaB through c-FLIP-L expression
Authors: Valérie Benoit
Valérie Deregowski
Laurence Delacroix
Nathalie Jacobs
Alain Chariot
Marie-Paule Merville
Vincent Bours
Journal: Cancer research (2004)
Discipline: CLINICAL MEDICINE
Keywords: oncoprotein; HER-2/neu; caspase-8; TNF-alpha; breast cancer
Affiliations: Laboratory of Medical Chemistry and Human Genetics, Center for Molecular and Cellular Therapy and Center for Research in Experimental Cancerology, University of Liege, Liege, Belgium.

Abstract:  The oncoprotein HER-2/neu is a prosurvival factor, and its overexpression has been correlated with poor prognosis in patients with breast cancer. We report that HER-2 is a new substrate for caspase-8 and that tumor necrosis factor alpha (TNF-alpha) stimulation leads to an early caspase-8-dependent HER-2 cleavage in MCF7 A/Z breast adenocarcinoma cells defective for nuclear factor kappaB (NFkappaB) activation. We show that the antiapoptotic transcription factor NFkappaB counteracts this cleavage through induction of the caspase-8 inhibitor c-FLIP. Our results also demonstrate that this HER-2 cleavage contributes to the TNF-alpha-induced apoptosis pathway because ectopic expression of an uncleavable HER-2 protects NFkappaB-defective cells against TNF-alpha-mediated cell death. Therefore, we propose an original model in which NFkappaB exerts a new antiapoptotic function by counteracting TNF-alpha-triggered cleavage of the HER-2 survival factor. 

Retracted: No

PubPeer comments:
 Retracted, [29 December 2021] . H t [RetractionWatch] . ----------------------------------- The journal and Chief Editors retract the 25 March 2021 article cited above.u200b Following publication, concerns were raised regarding the validity of the data in the article. The authors failed to provide the raw data or a satisfactory explanation during the investigation, which was conducted in accordance with Frontiersu2019 policies. Given the concerns, and the lack of raw data, the editors no longer have confidence in the findings presented in the article. u200b This retraction was approved by the Chief Editors of Frontiers in Oncology and the Chief Executive Editor of Frontiers. The authors have not responded to any correspondence regarding the retraction. --------------------------- It would be interesting to learn more about the  concerns that were raised , and who raised them. This is Fig 5A ( Tumors were isolated after injection of H1650 cells ), in which the tumor images stripped of their backgrounds and collaged onto a black background, so that one can only speculate about their actual sizes. ![file] ,
miR-128 downregulation promotes growth and metastasis of bladder cancer cells and involves VEGF-C upregulation
Authors: Xiong-Bing Zu
Jinbo Chen
X U Zhou
Y U Cui
Shiyu Tong
Zhi Chen
Lin Qi
Tianxiang Huang
Journal: Oncology Letters (2015)
Discipline: CLINICAL MEDICINE
Keywords: bladder cancer; metastasis; miR-128; vascular endothelial growth factor-C.
Affiliations: Department of Urology, Xiangya Hospital, Central South University, Changsha, Hunan 430121, P.R. China., Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 430121, P.R. China.

Abstract:  MicroRNA-128 (miR-128) serves an important role in regulating growth, invasiveness, stem cell-like traits, differentiation and apoptosis of different types of tumor cells. Vascular endothelial growth factor-C (VEGF-C) has been associated with angiogenesis, lymphangiogenesis and regional lymph node metastasis and has previously been reported to have an anti-apoptotic and proliferative role in bladder cancer (BC). To investigate the regulation of miR-128 on VEGF-C expression and their effects on proliferation and metastasis of bladder cancer, T24 and 5637 BC cells were transfected with pre-miR-128, anti-miR-128 and their respective negative control. miR-128 was downregulated in BC tissues and cell lines, while the expression levels of VEGF-C were upregulated. The present results indicated that miR-128 negatively regulated VEGF-C expression in BC T24 and 5637 BC cells. VEGF-C is a direct target of miR-128 in BC cells. Overexpression of miR-128 inhibited cell proliferation, migration and invasion. Knockdown of miR-128 promoted proliferation, migration and invasion in BC cells. Therefore, downregulation mediated malignant progression of BC may be partly attributed to increased VEGF-C expression. Consequently, the findings of the present study provide a molecular basis for the role of miR-128/VEGF-C in the progression of human BC and indicate a novel target for treatment of BC. 

Retracted: No

PubPeer comments:
 Fig 6B.  The invasion capabilities of... (B) 5637 cells were measured by Transwell assay. Overlaps marked. ![file] ,
Hepatic glucagon action is essential for exercise-induced reversal of mouse fatty liver
Authors: Clinton M Hasenour
Robert S Lee-Young
Daniel G Lustig
David H Wasserman
Richard A Baheza
Larry L Swift
Sara E Lynes
Eric D Berglund
Maureen J Charron
Bruce M Damon
E Patrick Donahue
Journal: Diabetes (2011)
Discipline: CLINICAL MEDICINE
Keywords: Exercise; fatty liver; glucagon action; hepatic; mice
Affiliations: Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, USA. 

Abstract:  Objective: Exercise is an effective intervention to treat fatty liver. However, the mechanism(s) that underlie exercise-induced reductions in fatty liver are unclear. Here we tested the hypothesis that exercise requires hepatic glucagon action to reduce fatty liver. Research design and methods: C57BL/6 mice were fed high-fat diet (HFD) and assessed using magnetic resonance, biochemical, and histological techniques to establish a timeline for fatty liver development over 20 weeks. Glucagon receptor null (gcgr(-/-)) and wild-type (gcgr(+/+)) littermate mice were subsequently fed HFD to provoke moderate fatty liver and then performed either 10 or 6 weeks of running wheel or treadmill exercise, respectively. Results: Exercise reverses progression of HFD-induced fatty liver in gcgr(+/+) mice. Remarkably, such changes are absent in gcgr(-/-) mice, thus confirming the hypothesis that exercise-stimulated hepatic glucagon receptor activation is critical to reduce HFD-induced fatty liver. Conclusions: These findings suggest that therapies that use antagonism of hepatic glucagon action to reduce blood glucose may interfere with the ability of exercise and perhaps other interventions to positively affect fatty liver. 

Retracted: Yes

PubPeer comments:
null, 
null, 
null, 
null, 
null, 
null, 
null, 
null, 
 Retraction Watch wrote about this case: https: retractionwatch.com 2016 11 02 author-pulls-diabetes-paper-with-duplicated-western-blots ,
Fibroblast growth factor 21 reverses suppression of adiponectin expression via inhibiting endoplasmic reticulum stress in adipose tissue of obese mice
Authors: Hongzhi Sun
Bo Zhou
Jiali Liu
Huixia Li
Shufang Wu
Lin Xu
Qinyue Guo
Journal: Experimental Biology and Medicine (2017)
Discipline: CLINICAL MEDICINE
Keywords: Adiponectin; endoplasmic reticulum stress; fibroblast growth factor 21; insulin resistance; obese mice
Affiliations: 1 Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China., 2 Department of Endocrinology, the Affiliated Guangren Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, China., 3 Clinical Laboratory, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China., 4 Key Laboratory of Environment and Genes Related to Diseases, Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China., 5 Center for Translational Medicine, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, China.

Abstract:  Fibroblast growth factor 21 (FGF21) has recently emerged as a novel endocrine hormone involved in the regulation of glucose and lipid metabolism. However, the exact mechanisms whereby FGF21 mediates insulin sensitivity remain not fully understood. In the present study, FGF21was administrated in high-fat diet-induced obese mice and tunicamycin-induced 3T3-L1 adipocytes, and metabolic parameters, endoplasmic reticulum (ER) stress indicators, and insulin signaling molecular were assessed by Western blotting. The administration of FGF21 in obese mice reduced body weight, blood glucose and serum insulin, and increased insulin sensitivity, resulting in alleviation of insulin resistance. Meanwhile, FGF21 treatment reversed suppression of adiponectin expression and restored insulin signaling via inhibiting ER stress in adipose tissue of obese mice. Additionally, suppression of ER stress via the ER stress inhibitor tauroursodeoxycholic acid increased adiponectin expression and improved insulin resistance in obese mice and in tunicamycin-induced adipocytes. In conclusion, our results showed that the administration of FGF21 reversed suppression of adiponectin expression and restored insulin signaling via inhibiting ER stress under the condition of insulin resistance, demonstrating the causative role of ER stress in downregulating adiponectin levels. 

Retracted: No

PubPeer comments:
 ![file] ![file] These blots are identical. , 
 I am not sure that I agree with #1. The lanes marked in red look different to me. And, although the two images posted are identical, they appear to both show Figure 2F. ,
ING2 controls the progression of DNA replication forks to maintain genome stability
Authors: Delphine Larrieu
Elisabeth Brambilla
Sagar Sengupta
Damien Ythier
Romuald Binet
Christian Brambilla
Rémy Pedeux
Journal: EMBO Reports (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ING2; tumour suppressor gene; DNA replication; genome stability; proliferating cell nuclear antigen
Affiliations: Molecular Bases of Lung Cancer Progression, INSERM U823, Institut Albert Bonniot, Université Joseph Fourier Grenoble 38706 Cedex France, National Institute of Immunology, Aruna Asaf Ali Marg New Delhi 110067 India, INSERM U917, IFR140, Faculté de Médecine, Université de Rennes 1 35043 Rennes Cedex France

Abstract:  Inhibitor of growth 2 (ING2) is a candidate tumour suppressor gene the expression of which is frequently lost in tumours. Here, we identified a new function for ING2 in the control of DNA replication and in the maintenance of genome stability. Global replication rate was markedly reduced during normal S-phase in small interfering RNA (siRNA) ING2 cells, as seen in a DNA fibre spreading experiment. Accordingly, we found that ING2 interacts with proliferating cell nuclear antigen and regulates its amount to the chromatin fraction, allowing normal replication progression and normal cell proliferation. Deregulation of DNA replication has been previously associated with genome instability. Hence, a high proportion of siRNA ING2 cells presented endoreduplication of their genome as well as an increased frequency of sister chromatid exchange. Thus, we propose for the first time that ING2 might function as a tumour suppressor gene by directly maintaining DNA integrity. 

Retracted: No

PubPeer comments:
 Figure 3A. Much more similar than you would expect. https: imgur.com I33ggTL ,
TGF-β1/Smad3 Signaling Pathway Suppresses Cell Apoptosis in Cerebral Ischemic Stroke Rats
Authors: Jian Jiang
Qunfeng Gui
Huaqun Chen
Xiaoyang Sun
Haiping Zhu
Xiaobo Hui
Lianshu Ding
Xiaodong Wang
Yanping Wang
Journal: Medical Science Monitor (2017)
Discipline: CLINICAL MEDICINE
Keywords: Transforming growth factor-β1; Smad3; hippocampus; cerebral ischemic stroke; nerve cells
Affiliations: Department of Neurosurgery, The First People's Hospital of Changshou City, Changshou, Jiangsu, China (mainland)., Department of Neurosurgery, Yancheng Third People's Hospital, The affiliated Yancheng Hospital of Southeast University Medical College, Yancheng, Jiangsu, China (mainland)., Department of Neurosurgery, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China (mainland).

Abstract:  BACKGROUND We desired to observe the changes of transforming growth factor-β1/drosophila mothers against decapentaplegic protein (TGF-β1/Smad3) signaling pathway in the hippocampus region of cerebral ischemic stroke rats so that the effects of this pathway on nerve cells can be investigated. MATERIAL AND METHODS The ischemic stroke models were built by middle cerebral artery occlusion (MCAO) in vivo and oxygen-glucose deprivation (OGD) in vitro. TGF-β1 and TGF-β1 inhibitors were injected into rat models while TGF-β1, TGF-β1 siRNA, Smad3, and Smad3 siRNA were transfected into cells. Infarct sizes were measured using triphenyltetrazolium chloride (TTC) staining, while the apoptosis rate of cells were calculated by Annexin V-fluorescein isothiocyanate/propidium iodide (Annexin V-FITC/PI) staining. Levels of TGF-β1, Smad3, and Bcl-2 were examined by real-time polymerase chain reaction (RT-PCR), immunohistochemical, and Western blot analysis. RESULTS The expressions of TGF-β1/Smad3 signal pathway were significantly increased in both model rats and BV2 cells, whereas the expression of Bcl-2 was down-regulated (P&lt;0.05). The TGF-β1/Smad3 signal pathway exhibited protective effects, including the down-regulation of infarction size in cerebral tissues and the down-regulation of apoptosis rate of BV2 cells by increasing the expression of Bcl-2 (P&lt;0.05). In addition, these effects could be antagonized by the corresponding inhibitors and siRNA (P&lt;0.05). CONCLUSIONS The TGF-β1/Smad3 signaling pathway was up-regulated once cerebral ischemic stroke was simulated. TGF-β1 may activate the expression of Bcl-2 via Smad3 to suppress the apoptosis of neurons. 

Retracted: No

PubPeer comments:
 Fig 7.  Apoptosis rate of cells in each group estimated by flow cytometry. (Au2013F) Distribution of apoptotic cells in groups of control (A), OGD (B), TGF-b1 (C), TGF-b1 siRNA (D), Smad3 (E), and Smad3 siRNA (F). ![file] Could the authors comment on the similarity to Fig 5 of [Liu, Du Ruan (2017)] ? ![] , 
 Fig 3.  Immunohistochemical staining with Smad3 in brain tissues for groups of normal (A), sham (B), model (C), TGF-b1 (D), and TGF-b1 inhibitors (E). Note the surprising similarity of A and B, after a 180-deg flip. ![] Other motifs repeated between A and E are marked. ,
miR-143 suppresses the osteogenic differentiation of dental pulp stem cells by inactivation of NF-κB signaling pathway via targeting TNF-α
Authors: Guofang Wang
Peng Zhang
Yajing Li
Wenli Yang
Journal: Archives of oral biology (2018)
Discipline: CLINICAL MEDICINE
Keywords: Dental pulp stem cells; NF-κB signaling pathway; Osteogenic differentiation; TNF-α; miR-143.
Affiliations: Department of Prosthodontics, The First Affiliated Hospital & School of Stomatology, Zhengzhou University, No. 40 Daxue Road, Zhengzhou, 450052, China. Electronic address: ., Department of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China., Department of Periodontology, The First Affiliated Hospital & School of Stomatology, Zhengzhou University, Zhengzhou, 450052, China.

Abstract:  Background: Dental pulp stem cells (DPSCs) are multipotent and play an important role in repairing damaged and/or defective dentinogenesis/osteogenesis. Recent studies have documented the implication of miR-143 in osteogenic differentiation of DPSCs. Nevertheless, the detailed mechanisms of miR-143 involved in the osteogenic differentiation of DPSCs remain to be further elaborated. Methods: Isolated DPSCs were incubated with osteogenic differentiation medium to induce osteogenic differentiation. qRT-PCR and western blot were performed to determine the expressions of miR-143 and tumor necrosis factor α (TNF-α). Luciferase reporter assay was used to confirm whether TNF-α was a target of miR-143. Osteogenic differentiation of DPSCs was evaluated by alkaline phosphatase (ALP) activity assay, ALP staining, and western blot analyses of osteogenic-markers including bone morphogenetic protein 2 (BMP2), ALP, runt-related transcription factor 2 (RUNX2) and collagen type I (COLI). Results: miR-143 was downregulated and TNF-α was upregulated during osteogenic differentiation of DPSCs. miR-143 posttranscriptionally regulated TNF-α expression in DPSCs by binding to its 3'UTR. miR-143 overexpression suppressed osteogenic differentiation of DPSCs, as demonstrated by the decrease of ALP activity, ALP positive cell ratio, as well as BMP2, ALP, RUNX2, and COLI expressions. Moreover, miR-143 reversed TNF-α-induced osteogenic differentiation of DPSCs. Finally, the osteogenic differentiation of DPSCs induced by miR-143 inhibitor was attenuated following inactivation of nuclear factor kappa B (NF-κB) signaling pathway. Conclusion: miR-143 suppressed the osteogenic differentiation of DPSCs by blockade of NF-κB signaling pathway via targeting TNF-α. 

Retracted: No

PubPeer comments:
 Figs 5E, 4E, 3E. A single versatile beta-actin loading control appears to be serving three different purposes. ![file] ,
Magnolol treatment reversed the glial pathology in an unpredictable chronic mild stress-induced rat model of depression
Authors: Lu-Fan Li
Jie Yang
Rong Qu
Shi-Ping Ma
Journal: European Journal of Pharmacology (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: glia atrophy; major depressive disorder; Magnolol; antidepressant-like effect; mechanisms
Affiliations: State Key of Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing 210009, China.

Abstract:  Growing evidence indicates that glia atrophy contributes to the pathophysiology and the pathogenesis of major depressive disorder. Magnolol is the main constituent identified in the bark of Magnolia officinalis, which has been used for the treatment of mental disorders, including depression, in Asian countries. In this study, we investigated the antidepressant-like effect and the possible mechanisms of magnolol in rats subjected to unpredictable chronic mild stress (UCMS). The ameliorative effect of magnolol on depression symptoms was investigated through behavior tests, including sucrose preference test, open-field test and forced-swimming test. In addition, the levels of glial fibrillary acidic protein (GFAP), an astrocyte marker, in the hippocampus and prefrontal cortex were determined by immunohistochemistry, Western blot, and reverse transcription-polymerase chain reaction (RT-PCR). Exposure to UCMS resulted in a decrease of behavioral activity, whereas magnolol (20, 40 mg/kg) and fluoxetine (20mg/kg) administration significantly reversed the depressive-like behaviors (P&lt;0.05).Moreover, treatment with magnolol effectively increased GFAP mRNA and protein levels in UCMS rats. These results confirmed the antidepressant-like effect of magnolol, which maybe primarily mediated by reversing the glial atrophy in the UCMS rat brain. 

Retracted: No

PubPeer comments:
 There are numerous small duplications in the images of Figure 6. It is as if certain stained neurons have been copied to give an impression of more or less dense staining in the images. Here are a couple of easy-to-make-out examples from panel A: ![file] There are also some obvious duplications in panel F: ![file] Some duplications are so subtle they are hard to point out. However, none of these should be occurring. Can the authors explain? ,
Parallel Implementation of the Deterministic Ensemble Kalman Filter for Reservoir History Matching
Authors: Tomas Pieler
Annette Borchers
Journal: Processes (2021)
Discipline: CHEMISTRY
Keywords: Xenopus embryos; pluripotent cells; organogenesis; human embryonic stem cells; animal cap cells

Abstract:  Xenopus embryos provide a rich source of pluripotent cells that can be differentiated into functional organs. Since the molecular principles of vertebrate organogenesis appear to be conserved between Xenopus and mammals, this system can provide useful guidelines for the directional manipulation of human embryonic stem cells. Pluripotent Xenopus cells can be easily isolated from the animal pole of blastula stage Xenopus embryos. These so called "animal cap" cells represent prospective ectodermal cells, but give rise to endodermal, mesodermal and neuro-ectodermal derivatives if treated with the appropriate factors. These factors include evolutionary conserved modulators of the key developmental signal transduction pathways that can be supplied either by mRNA microinjection or direct application of recombinant proteins. This relatively simple system has added to our understanding of pancreas, liver, kidney, eye and heart development. In particular, recent studies have used animal cap cells to generate ectopic eyes and hearts, setting the stage for future work aimed at programming pluripotent cells for regenerative medicine. 

Retracted: No

PubPeer comments:
 In a series of MDPI papers, this paper too shows non-relevant references to the subject at hand. For example, the references [17] and [24] are irrelevant to the Formulas boxed in the text below as the formulas were not found in either one of the arbitrarily indicated references [17,24]! ![file] ![file] It might be worth mentioning that the last co-author of this paper **( Zhangxing Chen)** is also the Guest Editor of the same Special Issue that the paper published in **MDPI Processes:** ![file] ![file] There is a typo in his name, as it is **( Zhangxing Chen)** instead of **( Zhangxin Chen)**! , 
 #1 Thanks for the comments. (1) For the Equation X5 in our paper, you can find it in Eq. 1.20 in page 11 of the Enkf-C user guide on https: arxiv.org abs 1410.1233 or in the file enkf-userguide.pdf on https: github.com sakov enkf-c tree master enkf in the folder enkf doc (2) For the Equation w in our paper, please refer to Ref.[17]. It can be obtained from the Eq. (1), (3) and (4) by substituting (3) and (4) into (1). (3) Zhangxing Chen is the official name of Dr. Chen and he uses Zhangxin Chen in his publications. Yes, he is one of the editors for this special issue. Lihua Shen ,
Exosomal miR-106b serves as a novel marker for lung cancer and promotes cancer metastasis via targeting PTEN
Authors: Lei Chen
Chenlei Xu
Qiaoli Zhang
Zaichun Deng
Qunli Ding
Shifang Sun
Yun Zhang
Hailin Chen
Journal: Life Sciences (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Exosome; Invasion; Lung cancer; Migration; PTEN
Affiliations: Department of Respiratory, The Affiliated Hospital of Medical School of Ningbo University., Department of Clinical Laboratory, The Affiliated Hospital of Medical School of Ningbo University., Department of Clinical Pharmacology, The Affiliated Hospital of Medical School of Ningbo University., Department of Respiratory, The Affiliated Hospital of Medical School of Ningbo University. Electronic address: .

Abstract:  As novel non-invasive tumor diagnostic biomarkers, exosomal bioactive miRNAs have received increasing attention. Herein, the aim of this study is to explore the clinical values and roles of exosomal miR106b in lung cancer. The exosomal miR-106b level was much higher in the serum of patients with lung cancer than that in healthy volunteers. Also, the exosomal miR-106b level in the lung cancer patient serum was associated with TNM stages and lymph node metastasis. Furthermore, exosomal miR-106b enhanced the migrated and invasive ability of lung cancer cells and increased the MMP-2 and MMP-9 expression. Mechanistically, exosomal miR-106b could target PTEN, and promote lung cancer cell migration and invasion. More importantly, PTEN overexpression reversed the effect of exosomal miR-106b on lung cancer cell migration and invasion. Taken together, these findings indicate that exosomal miR-106b may be a promising diagnostic biomarker and drug target for patients with lung cancer. 

Retracted: No

PubPeer comments:
 Two images in Figure 2A appear to overlap. Contrast and cropping appear to be different. Corresponding authoru2018s email address is numerical, and bears no resemblance to the authoru2019s name. *** ![file] , 
 An image in 2D and 4G appear to be the same, with different contrast. Could the authors please review to see if they should be the same; they seem to be described differently. *** ![file] *** ![file] *** ![file] , 
 An image in Figures 3 and 4 appear to overlap, but appear to be differently described. There may be other overlapping issues in this paper, but perhaps the authors could check. *** ![file] , 
 There appears to be image overlap between 2 papers: Aging (2020) doi: 10.18632 aging.104000 and Journal of Cancer (2019) doi: 10.7150 jca.33765. Aging paper has a thread too: https: pubpeer.com publications 16C458681B5B9884E96BBD13B5FFCF Could the authors comment? Apologies if I m misunderstanding something. Please ignore the orange boxes. *** *** ![file] *** ![file] ,
Context dependent splicing functions of Bud31/Ycr063w define its role in budding and cell cycle progression
Authors: Debjani Saha
Usha Vijayraghavan
Samirul Bashir
Shataparna Banerjee
Journal: Biochemical and Biophysical Research Communications (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Yeast; Bud31; spliceosome assembly; pre-mRNA splicing; cell cycle transitions
Affiliations: Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560012, India.

Abstract:  The yeast Bud31 protein, a Prp19 complex (NTC) member, aids spliceosome assembly and thus promotes efficient pre-mRNA splicing. The bud31 null cells show mild budding abnormalities at optimal growth temperatures and, at higher temperatures, have growth defects with aberrant budding. Here we have assessed cell cycle transitions which require Bud31. We find Bud31 facilitates passage through G1-S regulatory point (Start) but is not needed for G2-M transition or for exit from mitosis. To co-relate Bud31 functions in cell division with splicing, we studied the splicing status of transcripts that encode proteins involved in budding. We find Bud31 promotes efficient splicing of only some of these pre-mRNAs, for example, ARP2 and SRC1. Wild type cells have a long and a short isoform of SRC1 mRNA and protein, out of which the shorter mRNA splice variant is predominant. bud31Δ cells show inefficient SRC1 splicing and entirely lack the shorter SRC1 spliced mRNA isoform. Yeast PRP17, another NTC sub-complex member, is also required for G1-S and G2-M cell cycle transitions. We examined genetic interactions between BUD31 and PRP17. While both factors were needed for efficient cell cycle dependent gene expression, our data indicate that distinct pre-mRNAs depend on each of these non-essential splicing factors. 

Retracted: No

PubPeer comments:
 ![file] , 
 Fig 4 A. The phenotype of prp17u0394 is lethality at any temperature above 33C, hence results shown in panel marked 34C is the relevant data. The right most panel 37C is irrelevant and superfluous and should not have been there. The result that over-expression of BUD31 in prp17u0394 mutant cells does not rescue the temperature sensitivity is apparent from panel 340 C. This matches the conclusion stated that these two factors of the NTC and Cef1p complex (Bud31 and Prp17) show no genetic redundancy. , 
 Fig 4 A. The phenotype of prp17u0394 is lethality at any temperature above 33C, hence results shown in panel marked 34C is the relevant data. The right most panel ****37C is irrelevant and superfluous and should not have been there. The result that over-expression of BUD31 in prp17u0394 mutant cells does not rescue the temperature sensitivity is apparent from panel 34C. This matches the conclusion stated that these two factors of the NTC and Cef1p complex (Bud31 and Prp17) show no genetic redundancy. ,
Ectopic expression of Bcl-XL or Ku70 protects human colon cancer cells (SW480) against curcumin-induced apoptosis while their down-regulation potentiates it
Authors: Ramachandran Rashmi
Santhosh Kumar
Devarajan Karunagaran
Journal: Carcinogenesis (2004)
Discipline: CLINICAL MEDICINE
Keywords: Curcumin; apoptosis; cancer cells; Bcl-XL; Ku70
Affiliations: Division of Cancer Biology, Rajiv Gandhi Center for Biotechnology, Thiruvananthapuram, Kerala 695014, India.

Abstract:  Curcumin, the yellow pigment derived from Curcuma longa, is known to induce apoptosis of several cancer cells. However, many cancer cells protect themselves by over-expressing antiapoptotic proteins such as Bcl-XL or Ku70. To study their role in curcumin-induced apoptosis, human colon cancer cells (SW480) were made to over-express or under-express Bcl-XL (by stable transfection) and Ku70 (by transient transfection) using plasmid constructs that express their genes in sense or antisense orientation, respectively. Stable cells that express Bax [Bax-GFP (green fluorescent protein)], a proapoptotic member of the Bcl-2 family, were also established. Curcumin-induced cell death and nuclear condensation was more in AsBcl-XL and AsKu70 cells that under-express Bcl-XL and Ku70, respectively, compared with the vector-transfected cells. Bcl-XL and Ku70 protected the cells by inhibiting the release of cytochrome c, Smac (second mitochondria derived activator of caspase) and apoptosis inducing factor (AIF), and the activation of caspases 9, 8 and 3 triggered by curcumin. AsBcl-XL and AsKu70 cells were more sensitive to curcumin through enhanced activation of caspases 9 and 3 and release of cytochrome c, Smac and AIF. Curcumin-induced activation of caspase 8 was blocked by Ku70 but not by Bcl-XL. However, caspase 8 activation by curcumin was accelerated in both AsBcl-XL and AsKu70 cells suggesting a possible feedback activation of caspase 8 by caspase 3. Bax-GFP cells were highly sensitized when Ku70 was down-regulated supporting the reported role of Ku70 in the retention of Bax within the cytosol. The study reveals the potential of antisense inhibition of antiapoptotic proteins as an effective strategy to tackle chemoresistant cancers with curcumin. 

Retracted: No

PubPeer comments:
 Figure 5A appears to have two images which overlap, although it seems they are supposed to represent two different cell types. *** ![file] ![file] ,
The circadian clock gene PER2 plays an important role in tumor suppression through regulating tumor-associated genes in human oral squamous cell carcinoma
Authors: Kai Yang
Qin Zhao
Dan Zhao
Xiaoli Su
Xiaoqiang Lv
Yiran Ao
Dan Chen
Journal: Oncology Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: clock gene; PER2; carcinogenesis; cancer development; RNA interference
Affiliations: Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Chongqing Medical University, Yuzhong, Chongqing 400016, P.R. China.

Abstract:  Low expression of the clock gene PER2 is closely related to carcinogenesis and the development of cancer; however, the mechanism of the low expression of PER2 that led to cell malignant transformation remains unclear. This study used RNA interference (RNAi) technology to silence PER2 in SCC15 human oral squamous cell carcinoma (OSCC) cells. Then it was found that the ability of cancer cell proliferation, migration, and invasion were markedly increased (P&lt;0.05), and the ability of cancer cell apoptosis and the number of cells in G1/G0 phase were markedly reduced (P&lt;0.05) after PER2 knockdown. PER2 knockdown increased the expression of Ki-67, MDM2, c-Myc, Bcl-2, MMP2, and VEGF mRNA (P&lt;0.05), and decreased the expression of p53, Bax, and TIMP-2 mRNA (P&lt;0.05). The in vivo experiments also proved that the tumorigenicity of SCC15 cells was significantly enhanced after PER2 silence (P&lt;0.05). Overall, these results show that PER2 through the regulation of the numerous important downstream tumor-related genes, plays a major role in tumor suppression, and it may be a novel molecular target for cancer treatment. 

Retracted: No

PubPeer comments:
 Figure 6B. * Red boxes. The PER2-shRNA-I and SCC15 panels appear to show an overlap. ![file] , 
 #1 About Figure 6 B in our paper, we have carefully checked our original data and pictures. We confirm that there is no error in the picture of the PER2-shRNA-I group in Fig. 6B, but there is indeed an error in the picture of the SCC15 group. This is due to our negligence and mistakenly placed another PER2-shRNA-I group picture in the position of the SCC15 group picture. We have contacted the editorial department of the magazine to revise it with the correct picture. We confirm that the mistake in original Fig. 6B does not affect the results and conclusions of this study. ,
Sustained delivery of chondroitinase ABC by poly(propylene carbonate)-chitosan micron fibers promotes axon regeneration and functional recovery after spinal cord hemisection
Authors: Tongliang Xia
Hongxu Qi
Jiangang Wang
Shilei Ni
Xiaodong Zhu
Shanying Huang
Xingang Li
Journal: Brain Research (2015)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: ChABC; Chitosan; Electrospinning; PPC; Spinal cord injury.
Affiliations: Department of Neurosurgery, Qilu Hospital, Shandong University, 107# Wenhua Xi Road, Jinan 250012, PR China., Institute of Polymer Science & Engineering, Tsinghua University, 30# Shuangqing Road, Beijing 100084, PR China., Key laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Health and Education, 107# Wenhua Xi Road, Jinan 250012, PR China., Department of Neurosurgery, Qilu Hospital, Shandong University, 107# Wenhua Xi Road, Jinan 250012, PR China. Electronic address: .

Abstract:  We describe the sustained delivery of chondroitinase ABC (ChABC) in the hemisected spinal cord using polypropylene carbonate (PPC) electrospun fibers with chitosan (CS) microspheres as a vehicle. PPC and ChABC-loaded CS microspheres were mixed with acetonitrile, and micron fibers were generated by electrospinning. ChABC release was assessed in vitro with high-performance liquid chromatography (HPLC) and revealed stabilized and prolonged release. Moreover, the released ChABC showed sustained activity. PPC-CS micron fibers with or without ChABC were then implanted into a hemisected thoracic spinal cord. In the following 4 weeks, we examined functional recovery and performed immunohistochemical analyses. We found that sustained delivery of ChABC promoted axon sprouting and functional recovery and reduced glial scarring; PPC-CS micron fibers without ChABC did not show these effects. The present findings suggest that PPC-CS micron fibers containing ChABC are a feasible option for spinal cord injury treatment. Furthermore, the system described here may be useful for local delivery of other therapeutic agents. 

Retracted: No

PubPeer comments:
 In Figure 2H, I, a micrograph has been duplicated and presented as something else. Another micrograph (Figure 2e) has also been reused from an earlier publication (Xia T et al., 2013; Brain Research; Figure 2c). In addition, there are some suspicious repetitions of numbers in Table 1 and 3, and across the two tables. ![file] ,
Clinical significance of CMTM4 expression in hepatocellular carcinoma
Authors: Xiaonian Zhu
Zhigang Wang
Chunhua Bei
Ying Zhang
Wen Zeng
Shengkui Tan
Riming Wei
Qiuyue Chen
Journal: OncoTargets and Therapy (2017)
Discipline: CLINICAL MEDICINE
Keywords: chemokine-like factor-like MARVEL transmembrane domain-containing 4; hepatocellular carcinoma; immunohistochemistry; prognosis.
Affiliations: Department of Epidemiology and Statistics, School of Public Health, Guilin Medical University., Department of Hepatobiliary Surgery, The Affiliated Hospital of Guilin Medical University., Department of Pathology, 181st Hospital of Chinese People's Liberation Army, Guilin, People's Republic of China.

Abstract:  CMTM4 is the most conserved member of chemokine-like factor (CKLF)-like MARVEL transmembrane domain-containing (CMTM) family on chromosome 16q22.1, a locus that harbors a number of tumor-suppressor genes. In previous studies, CMTM4 was reported to be downregulated and exhibited tumor-suppressor activities by regulating cell growth and cell cycle in clear cell renal cell carcinoma. However, its roles in tumorigenesis of hepatocellular carcinoma (HCC) remain poorly studied. This study first investigated the expression of CMTM4 in HCC, and then examined the association between the expression of CMTM4 with the clinicopathological features and prognosis of HCC patients. It was found that CMTM4 was downregulated in HCC tissues, compared with matched adjacent nontumor tissues, as detected by immunohistochemistry. In addition, Kaplan-Meier survival analysis showed that the negative expression of CMTM4 was associated with decreased overall survival rates in patients with HCC. The results of this study suggest CMTM4 plays a role as a tumor suppressor in HCC and CMTM4 negative expression is a risk factor for poor prognosis of HCC. 

Retracted: No

PubPeer comments:
 Figure 1 contains the only raw data presented in this article. None of the zoomed in images seem to correspond with the sections selected from the original micrograph. ![file] ,
Circular RNA MTO1 inhibits gastric cancer progression by elevating PAWR via sponging miR-199a-3p
Authors: Lei Yang
Yingying Zhao
Feng Xu
Ruifeng Song
Weiwei Hao
Ya Li
Bing Chen
Binghua Sun
Journal: Cell Cycle (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PAWR; circMTO1; gastric cancer; miR-199a-3p.
Affiliations: Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou City, PR. China.

Abstract:  The effect of circular RNA MTO1 (circMTO1) signaling on the expression of miR-199a-3p in gastric carcinoma cells, and its effect on proliferation and apoptosis of gastric cancer cells were investigated in this study. RT-qPCR was performed to detect the expression levels of circMTO1 and miR-199a-3p in the cell lines and tissues of gastric cancer. The effect of circMTO1 and miR-199a-3p on the growth and apoptosis of tumor cells was detected by BrdU incorporation and Annexin V/PI staining. Target gene prediction and screening, and luciferase reporter assays were performed to validate downstream interested genes of circMTO1 and miR-199a-3p. The expression levels of miR-199a-3p target gene PAWR (named as PRKC apoptosis WT1 Regulator Protein) was measured by RT-qPCR and Western blotting. Tumor changes in mice were detected by transfecting circMTO1. The expression of circMTO1 was significantly downregulated in the cell lines and tissues of gastric cancer, and low expression levels of circMTO1 were closely associated with poor prognosis. Overexpression of circMTO1 inhibited tumor growth, enhanced apoptosis rate and decreased cell invasion and migration. There was a significant negative relationship between the expression levels of circMTO1 and miR-199a-3p in gastric cancer tissues. Inhibiting miR-199a-3p expression or overexpression of PAWR could decrease the promotive effects of knockdown of circMTO1 on the progression of gastric cancer, and a positive relationship was established between the expression of circMTO1 and PAWR. circMTO1 can regulate the growth of gastric cancer cells by regulating miR-199a-3p/PAWR axis, thus inhibiting the development and progression of gastric cancer. Abbreviation GC: Gastric cancer; circ RNA: Circular RNA; MTO1: mitochondrial translation optimized 1 homolog. 

Retracted: No

PubPeer comments:
 *[left]* Fig 2e.  The representative photo of tumor in subcutaneous site. Scale bar = 20 u00b5m . *[right]* Fig 8A from [Song et al (2019)] .  The images of tumor xenografts of nude mice injected with siSNHG8u2013transfected or si-scrambleu2013transfected cells . ![file] Is it possible that this part of the study was conducted by an outside laboratory, hence the appearance of what looks like the same ruler in both images? -------------------------------------- UPDATE. Another sighting! Fig 6B from [Wang et al (2020)] .  The representative image of tumor xenografts from groups sh-LBX2-AS1 and sh-NC. ![] , 
 #1 [right] Fig 8A from Song et al (2019).  The images of tumor xenografts of nude mice injected with siSNHG8u2013transfected or si-scrambleu2013transfected cells . The Song et al (2019) paper was retracted on [4 October 2021] , on account of coming from a papermill. ,
Long non‑coding RNA MIAT competitively binds miR‑150‑5p to regulate ZEB1 expression in osteosarcoma
Authors: Hao Jin
Zhiqiang Yin
Feng Dong
Xin Jin
Yang Li
Wenbo Wang
Weiguang Chai
Journal: Oncology Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: epithelial-mesenchymal transition; osteosarcoma.
Affiliations: Department of Orthopaedics, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150006, P.R. China.

Abstract:  Long non-coding RNAs (LncRNAs), are significant in a number of biological stages and illnesses. The myocardial infarction associated transcript (MIAT) serves a function in numerous types of illness and physiological and pathological processes, including paranoid schizophrenia, diabetic retinopathy, myocardial infarction and neuroendocrine prostate cancer. However, the function of the lncRNA MIAT in the development of osteosarcoma is unknown. It has been identified that during the development of osteosarcoma, MIAT is upregulated in tumor tissues compared to adjacent non-tumor tissues. The spreading and proliferation of osteosarcoma cells was reduced by MIAT knockdown. These findings indicate that MIAT functions by competing with critical RNAs to target miR-150-5p and activate zinc finger E-box binding homeobox 1 to modulate the function of osteosarcoma cells. Together, the present findings may contribute to the understanding of the pathogenesis of osteosarcoma. 

Retracted: No

PubPeer comments:
 Figure 2D. Panels share similarities to panels in Figure 4B of a different paper by different authors, but possibly the same hospital. That paper is: Yanfeng Li et al. - Oncology Reports 38: 3465-3472, 2017 - DOI: 10.3892 or.2017.6020 - https: pubpeer.com publications CF684DE973A8D88F0FE3F76A0A5C12 Similar groups of cells are shown here with boxes of the same color. Could the authors please explain what happened here? ![file] ,
Cooperation between snail and LEF-1 transcription factors is essential for TGF-beta1-induced epithelial-mesenchymal transition
Authors: Elizabeth D Hay
Daniel A Goodenough
Damian Medici
Journal: Molecular Biology of the Cell (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Transforming growth factor beta 1; epithelial-mesenchymal transition; E-cadherin; claudin-1; claudin-2
Affiliations: Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA., Department of Cell Biology, Harvard Medical School, Boston, MA 02115

Abstract:  Transforming growth factor beta 1 (TGF-beta1) has been shown to induce epithelial-mesenchymal transition (EMT) during various stages of embryogenesis and progressive disease. This alteration in cellular morphology is typically characterized by changes in cell polarity and loss of adhesion proteins such as E-cadherin. Here we demonstrate that EMT is associated with loss of claudin-1, claudin-2, occludin, and E-cadherin expression within 72 h of exposure to TGF-beta1 in MDCKII cells. It has been suggested that this expression loss occurs through TGF-beta1 in a Smad-independent mechanism, involving MEK and PI3K pathways, which have previously been shown to induce expression of the Snail (SNAI-1) gene. Here we show that these pathways are responsible for loss of tight junctions and a partial loss of E-cadherin. However, our results also demonstrate that a complete loss of E-cadherin and transformation to the mesenchymal phenotype are dependent on Smad signaling, which subsequently stimulates formation of beta-catenin/LEF-1 complexes that induce EMT. 

Retracted: No

PubPeer comments:
 Figure 3D. Much more similar than expected. ![file] Figure 4D. Much more similar than expected. ![file] Figure 4F. Much more similar than expected. ![file] Could the authors post the original full blots here? ,