PReD-Bench/PRed-Bench huggingface dataset:
Myostatin induces DNA damage in skeletal muscle of streptozotocin-induced type 1 diabetic mice
Authors: Mridula Sharma
Prasanna Kumar Juvvuna
Ravi Kambadur
Subha Subramanian
Sandhya Sriram
Craig McFarlane
Monica Senna Salerno
Journal: Journal of Biological Chemistry (2014)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: DNA; DNA Damage; Diabetes; Myostatin; Skeletal Muscle
Affiliations: From the Division of Molecular Genetics and Cell Biology, School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore 637551.

Abstract:  One of the features of uncontrolled type 1 diabetes is oxidative stress that induces DNA damage and cell death. Skeletal muscle atrophy is also considerable in type 1 diabetes, however, the signaling mechanisms that induce oxidative stress culminating in muscle atrophy are not fully known. Here, we show that in Streptozotocin-induced diabetic wild type mice, hypo-phosphorylation of Akt, resulted in activation of Foxa2 transcription factor in the muscle. Foxa2 transcriptionally up-regulated Myostatin, contributing to exaggerated oxidative stress leading to DNA damage via p63/REDD1 pathway in skeletal muscle of Streptozotocin-treated wild type mice. In Myostatin(-/-) mice however, Streptozotocin treatment did not reduce Akt phosphorylation despite reduced IRS-1 signaling. Moreover, Foxa2 levels remained unaltered in Myostatin(-/-) mice, while levels of p63/REDD1 were higher compared with wild type mice. Consistent with these results, relatively less DNA damage and muscle atrophy was observed in Myostatin(-/-) muscle in response to Streptozotocin treatment. Taken together, our results for the first time show the role of Foxa2 in Myostatin regulation in skeletal muscle in diabetic mice. Altogether, these results demonstrate the mechanism by which Myostatin contributes to DNA damage in skeletal muscle of the diabetic mice that would lead to myofiber degeneration. 

Retracted: Yes

PubPeer comments:
null, 
null, 
null, 
null, 
null, 
 https: www.straitstimes.com singapore 3-spore-based-scientists-linked-to-research-fraud , 
 #6 : old news, but the success story is from the first authors. Her company is thriving now. https: shiokmeats.com team ,
Expression of connexin 30 and connexin 32 in hippocampus of rat during epileptogenesis in a kindling model of epilepsy
Authors: Bijan Akbarpour
Mohammad Sayyah
Vahab Babapour
Reza Mahdian
Ahmad Reza Kamyab
Siamak Beheshti
Journal: Neuroscience Bulletin (2012)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Epileptogenesis; Connexins; Gap junctions; Hippocampus; Cx30
Affiliations: Department of Physiology, Pasteur Institute of Iran, Tehran 131694-3551, Islamic Republic of Iran.

Abstract:  Objective: Understanding the molecular and cellular mechanisms underlying epileptogenesis yields new insights into potential therapies that may ultimately prevent epilepsy. Gap junctions (GJs) create direct intercellular conduits between adjacent cells and are formed by hexameric protein subunits called connexins (Cxs). Changes in the expression of Cxs affect GJ communication and thereby could modulate the dissemination of electrical discharges. The hippocampus is one of the main regions involved in epileptogenesis and has a wide network of GJs between different cell types where Cx30 is expressed in astrocytes and Cx32 exists in neurons and oligodendrocytes. In the present study, we evaluated the changes of Cx30 and Cx32 expression in rat hippocampus during kindling epileptogenesis. Methods: Rats were stereotaxically implanted with stimulating and recording electrodes in the basolateral amygdala, which was electrically stimulated once daily at afterdischarge threshold. Expression of Cx30 and Cx32, at both the mRNA and protein levels, was measured in the hippocampus at the beginning, in the middle (after acquisition of focal seizures), and at the end (after establishment of generalized seizures) of the kindling process, by real-time PCR and Western blot. Results: Cx30 mRNA expression was upregulated at the beginning of kindling and after acquisition of focal seizures. Then it was downregulated when the animals acquired generalized seizures. Overexpression of Cx30 mRNA at the start of kindling was consistent with the respective initial protein increase. Thereafter, no change was found in protein abundance during kindling. Regarding Cx32, mRNA expression decreased after acquisition of generalized seizures and no other significant change was detected in mRNA and protein abundance during kindling. Conclusion: We speculate that Cx32 GJ communication in the hippocampus does not contribute to kindling epileptogenesis. The Cx30 astrocytic network localized to perivascular regions in the hippocampus is, however, overexpressed at the initiation of kindling to clear excitotoxic molecules from the milieu. 

Retracted: No

PubPeer comments:
 Figure 3 appears to have a repeated band, after vertical stretch. Difficult to understand how this could occur by accident during figure assembly. Shown below with enhanced contrast which better illustrates background similarities. ***  ,
RETRACTED ARTICLE: Blockage of miR-92a-3p with locked nucleic acid induces apoptosis and prevents cell proliferation in human acute megakaryoblastic leukemia
Authors: R Salehi
M Sharifi
Journal: Cancer Gene Therapy (2016)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; gene expression regulation; acute myeloid leukemia; miR-92a-3p; locked nucleic acid
Affiliations: Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Abstract:  MicroRNAs (miRNAs) are non-coding RNAs involved in post-transcriptional regulation of gene expression. In many cancers, up- or downregulation of different miRNAs is reported. In acute myeloid leukemia, upregulation of miR-92a-3p was reported in human in vitro studies. We performed blockage of miR-29a-3p in human acute megakaryoblastic leukemia cell line (M-07e) by using locked nucleic acid (LNA) and cell proliferation; apoptosis and necrosis were assessed. At different time points after LNA-anti-miR92a-3p transfection, miR-92a-3p quantitation was assessed by qRT-real-time PCR, MTT assay and annexin/propidium iodide staining were performed. The data were processed using the ANOVA test. At all three time points, the expression of miR-92a-3p was lower in the LNA-anti-miR group compared with the control groups. Cell viability between LNA-Anti-miR and the control group was statistically significant. Blockage of miR-92a-3p was associated with increment of the ratio of apoptotic cells in the LNA-anti-miR group was higher than the other group. The ratio of necrotic cells in the LNA-antimiR group was higher than the other groups. These assessments indicate that miR-92a-3p blockage can decrease the viability of M-07e cells, which is mainly due to induction of apoptosis and necrosis. Our findings could open up a path to a miRNA based therapeutic approach for treatment of acute megakaryoblastic leukemia. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: www.nature.com articles s41417-019-0158-y The Editor-in-Chief has retracted this article [1] because it overlaps significantly with three previous articles by the same author group [2,3,4]. Both authors disagree with this retraction. References 1. Sharifi M, Salehi R. Blockage of miR-92a-3p with locked nucleic acid induces apoptosis and prevents cell proliferation in human acute megakaryoblastic leukemia. Cancer Gene Ther. 2016;23:29u201335. 2. Sharifi M, Salehi M, Gheisari Y, Kazemi M. Inhibition of microRNA miR-92a induces apoptosis and necrosis in human acute promyelocytic leukemia. Adv Biomed Res. 2014;3:61. 3. Najafi Z, Sharifi M, Javadi G. Degradation of miR-21 induces apoptosis and inhibits cell proliferation in human hepatocellular carcinoma. Cancer Gene Ther. 2015;22:530u201335. 4. Sharifi M, Salehi R, Gheisari Y, Kazemi M. Inhibition of microRNA miR-92a induces apoptosis and inhibits cell proliferation in human acute promyelocytic leukemia through modulation of p63 expression. Mol Biol Res. 2014;41:2799u2013808. ,
Adeno-associated virus type 5 (AAV5) but not AAV2 binds to the apical surfaces of airway epithelia and facilitates gene transfer
Authors: R M Kotin
M Seiler
W Fulgeras
B L Davidson
J A Chiorini
R Walters
J Zabner
Journal: Journal of Virology (2000)
Discipline: MICROBIOLOGY
Keywords: cystic fibrosis; adeno-associated virus type 2 (AAV2); CFTR cDNA; airway epithelia; heparan sulfate proteoglycans
Affiliations: Departments of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA. , <!--label omitted: 1-->Departments of Internal Medicine1 and, <!--label omitted: 2-->Physiology &amp; Biophysics,2 University of Iowa College of Medicine, Iowa City, Iowa 52242, and, <!--label omitted: 3-->Laboratory of Molecular Hematology, National Heart, Lung, and Blood Institute,3 and, <!--label omitted: 4-->Gene Therapeutics Branch, National Institute for Dental and Craniofacial Research,4 National Institutes of Health, Bethesda Maryland 20892

Abstract:  In the genetic disease cystic fibrosis, recombinant adeno-associated virus type 2 (AAV2) is being investigated as a vector to transfer CFTR cDNA to airway epithelia. However, earlier work has shown that the apical surface of human airway epithelia is resistant to infection by AAV2, presumably as a result of a lack of heparan sulfate proteoglycans on the apical surface. This inefficiency can be overcome by increasing the amount of vector or by increasing the incubation time. However, these interventions are not very practical for translation into a therapeutic airway-directed vector. Therefore, we examined the efficiency of other AAV serotypes at infecting human airway epithelia. When applied at low multiplicity of infection to the apical surface of differentiated airway epithelia we found that a recombinant AAV5 bound and mediated gene transfer 50-fold more efficiently than AAV2. Furthermore, in contrast to AAV2, AAV5-mediated gene transfer was not inhibited by soluble heparin. Recombinant AAV5 was also more efficient than AAV2 in transferring beta-galactosidase cDNA to murine airway and alveolar epithelia in vivo. These data suggest that AAV5-derived vectors bind and mediate gene transfer to human and murine airway epithelia, and the tropism of AAV5 may be useful to target cells that are not permissive for AAV2. 

Retracted: No

PubPeer comments:
 Figure 1 appears to have two images which overlap. Roughly indicated with magenta boxes. *** False color  *** Original  ,
CarD is an essential regulator of rRNA transcription required for Mycobacterium tuberculosis persistence
Authors: Linda Chu
Christina L Stallings
Bryce E Nickels
Michael S Glickman
Nicolas C Stephanou
Ann Hochschild
Journal: Cell (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Mycobacterium tuberculosis; rRNA transcription; CarD; DksA; (p)ppGpp
Affiliations: Immunology Program, Sloan-Kettering Institute, New York, NY 10065, USA.

Abstract:  Mycobacterium tuberculosis is arguably the world's most successful infectious agent because of its ability to control its own cell growth within the host. Bacterial growth rate is closely coupled to rRNA transcription, which in E. coli is regulated through DksA and (p)ppGpp. The mechanisms of rRNA transcriptional control in mycobacteria, which lack DksA, are undefined. Here we identify CarD as an essential mycobacterial protein that controls rRNA transcription. Loss of CarD is lethal for mycobacteria in culture and during infection of mice. CarD depletion leads to sensitivity to killing by oxidative stress, starvation, and DNA damage, accompanied by failure to reduce rRNA transcription. CarD can functionally replace DksA for stringent control of rRNA transcription, even though CarD associates with a different site on RNA polymerase. These findings highlight a distinct molecular mechanism for regulating rRNA transcription in mycobacteria that is critical for M. tuberculosis pathogenesis. 

Retracted: No

PubPeer comments:
 Figure 4 (d) (e) show time series capture of electrical output generated by the device. However the time series seem to show time going backwards - what cannot be explained by any known instrument system.  Next in Figure 5 (c), the peaks are supposed to show different measurements obtained by changing the distance between device and source. When examining the signals they seem to all be versions of the same measurement: e.g. take the red curve and stretch to dimensions of the black curve - they look the same. Also compressing to dimensions of the blue curve.  ,
Lipoplexes versus nanoparticles: pDNA/siRNA delivery
Authors: Bharat Khurana
Amit K Goyal
Abhishek Budhiraja
Suresh P Vyas
Diasy Aora
Journal: Drug Delivery (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: siRNA; delivery system; chitosan nanoparticles; cationic liposomes; transfection efficiency
Affiliations: Department of Pharmaceutics, Nanomedicine Research Centre, Indo-Soviet Friendship College of Pharmacy, Moga, Punjab, India.

Abstract:  Small interfering RNA (siRNA) has been widely used as potential therapeutic for treatment of various genetic disorders. However, rapid degradation, poor cellular uptake and limited stability in blood limit the effectiveness of the systemic delivery of siRNA. Therefore, an efficient delivery system is required to enhance its transfection and duration of therapeutics. In the present study, plasmid DNA (pEGFPN3) expressing green fluorescent protein (GFP) was used as a reporter gene. Chitosan nanoparticles/polyplexes and cationic liposomes/lipoplexes were developed and compared for their transfectivity and therapeutic activity in mammalian cell line (HEK 293). The nanoparticulates were first characterized by assessing the surface charge (zeta potential), size (dynamic light scattering) and morphology (transmission electron microscope) followed by evaluation for their DNA retardation ability, transfection efficiency and cytotoxicity on HEK 293 cell line. The chitosan nanoparticles/plasmid DNA (pDNA) complex and liposomes/pDNA complex were co-transfected with GFP-specific siRNA into HEK 293 cells and it was found that both are efficient delivery vehicles for siRNA transfection, resulting in ~57% and ~70% suppression of the targeted gene (GFP), respectively, as compared with the mock control (cells transfected with nanocarrier/pDNA complexes alone). This strong inhibition of GFP expression indicated that cationic liposomes are better than chitosan nanoparticles and can be used as an effective carrier of siRNA in mammalian cells. 

Retracted: No

PubPeer comments:
 A niche medical application here. Did the patients incur kidney injury as a result of their cerebral hemorrhage, or vice versa, or were the two misfortunes independent?  Their prevention activity on the acute kidney injury in patients with acute cerebral hemorrhage is evaluated and the protentional mechanism is revealed Could the authors comment on the relevance of Refs [8, 9] in this context of coordination polymers? - [8] W. Liu, H. Li, H. Zhu, and P. Xu. Materials, 2020, 13, 1180. ** The Interfacial Adhesion Performance and Mechanism of a Modified Asphaltu2013Steel Slag Aggregate ** - [9] Z. Wang, X. Zhang, S. Jiang, Y. Qu, D. Ou, and J. Wang. J. Alloys Compd., 2020, 828, 154412. ** Arc erosion dynamic of island- and skeleton-restricted microstructure evolution modes in Agu2013CuO contact materials ** ,
Comparison of the properties of neural stem cells of the hippocampus in the tree shrew and rat in√Ø¬ø¬Ωvitro
Authors: Zi-Bin Zhang
Ting-Hua Wang
Piao Zhang
Xue-Rong Zhang
Liu-Lin Xiong
Rong-Ping Zhang
Yuan-Dong Hu
Qiong Zhao
Journal: Molecular Medicine Reports (2018)
Discipline: CLINICAL MEDICINE
Keywords: tree shrew; rat; neural stem cell; immunohistochemistry.
Affiliations: Institute of Neurological Disease, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China., Department of Anesthesiology, Sun Yat‚ÄëSen Memorial Hospital, Sun Yat‚ÄëSen University, Guangzhou, Guangdong 510120, P.R. China., Institute of Neuroscience, Kunming Medical University, Kunming, Yunnan 650031, P.R. China.

Abstract:  Neural stem cells (NSCs) are characterized by the ability of self‚Äërenewal and capacity to proliferate and produce new nervous tissue. NSCs are capable of differentiating to three lineages of neural cells, including neurons, oligodendrocytes and astrocytes. Furthermore, hippocampal NSCs transplantation can improve the neurological deficits associated with expression of cytokines. Therefore, to compare the properties of NSCs of tree shrews and rats in vitro, NSCs from tree shrews (tsNSCs) and rats f(rNSCs) were isolated. Nestin was used as a marker to identify the cultured NSCs. Neuronal nuclei protein and glial fibrillary acidic protein (GFAP) were utilized to demonstrate the differentiation of NSCs towards neurons and astrocytes, respectively, in vitro. Furthermore, the expression of neurotrophin 3 (NT3), brain‚Äëderived neurotrophic factor (BDNF), glial cell‚Äëderived neurotrophic factor (GDNF) and transforming growth factor (TGF)Œ≤1 was also investigated in tsNSCs and rNSCs. The expression of all of the aforementioned proteins was detected using immunofluorescence methods. The results demonstrated that, after 5 days of culture, the average number of neurospheres in the cultured tsNSCs was significantly lower compared with rNSCs (P=0.0031). Additionally, compared with the rNSCs, tsNSCs exhibited an enhanced differentiation ability towards neurons. Furthermore, the expression of NT3 in the tsNSCs was higher compared with rNSCs (P&lt;0.01), while the expression of BDNF was lower (P=0.045). However, no significant differences were observed in the expression level of GDNF and TGFŒ≤1 between rNSCs and tsNSCs. Therefore, these results indicate that tsNSCs exhibit specific characteristics that are different from rNSCs, which provides novel information for the understanding of NSCs obtained from tree shrews. Overall, the results of the current study provide evidence to support the increased application of tree shrews as models for diseases of the central nervous system. 

Retracted: No

PubPeer comments:
 Figure 3A. * Yellow, blue, and red boxes focus attention on pairs of panels that look unexpectedly similar  ,
Differential effects of bexarotene on intrinsic and extrinsic pathways in TRAIL-induced apoptosis in two myeloid leukemia cell lines
Authors: H J Deeg
Hans-Peter Kiem
David M Hockenbery
Shao Xu Ying
Xiao Li
Sudeshna Seal
John M Pagel
Nissa Abbassi
Ajay K Gopal
Journal: Leukemia & Lymphoma (2007)
Discipline: CLINICAL MEDICINE
Keywords: Tumor necrosis factor-related apoptosis-inducing ligand; TRAIL; apoptosis; retinoid receptor; RXR
Affiliations: Shanghai Sixth Hospital, Shanghai Jiaotong University, Shanghai, China.

Abstract:  Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces programmed cell death (apoptosis) preferentially in tumor cells. However, not all cancer cells are sensitive to TRAIL. We determined whether ligation of the retinoid receptor, RXR, would sensitize cells to TRAIL-mediated apoptosis. The leukemic cell lines KG1a (apoptosis-resistant) and ML-1 (apoptosis-sensitive) were treated with the RXR-specific retinoid bexarotene, TRAIL, or both, and apoptosis was determined. In KG1a cells, bexarotene downregulated FLIP(Long) and activated caspase-8, thereby allowing for TRAIL-triggered apoptosis. Overexpression of FLIP(Long) in ML-1 cells abrogated apoptosis. In unmodified ML-1 cells bexarotene enhanced programmed cell death via truncation of Bid and release of cytochrome C. Blockade of caspase-8 prevented enhancement in both cell lines; blockade of caspase-9 had a significant effect only in ML-1 cells. Thus, the effect of bexarotene on TRAIL-mediated programmed cell death involved proximal events of the extrinsic pathway; however, downstream signals involved the intrinsic pathway in ML-1 but not in KG1a cells. These studies add further information to the regulation of programmed cell death in leukemic cells that have to be considered when designing therapeutic strategies. 

Retracted: No

PubPeer comments:
 Concerns about Figure 2, reported to the journal in 2015. * Green boxes: The Actin panels representing 3h and 48h, respectively, appear to look very similar * Red boxes: Four lanes in the pro cleaved caspase lanes representing 18h and 48h, respectively, appear to look very similar  ,
A dual PI3K/AKT/mTOR signaling inhibitor miR-99a suppresses endometrial carcinoma
Authors: Zhenghua Xiao
Tangshu Luo
Ying Lin
Xiaojing Zhang
Zhongzu Zhang
Qin Zhou
Yunyun Li
Journal: American journal of translational research (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: PI3K/AKT/mTOR signaling pathway; endometrial carcinoma; miR-99a; microRNA.
Affiliations: Department of Gynecology and Obstetrics, The Yongchuan Hospital of Chongqing Medical University Chongqing 402160, PR China., Department of Orthopedics, The Yongchuan Hospital of Chongqing Medical University Chongqing 402160, PR China., Department of Gynecology and Obstetrics, The First Affiliated Hospital of Chongqing Medical University Chongqing 402160, PR China.

Abstract:  Activation of the PI3K/AKT/mTOR signaling pathway, a common mechanism in all subtypes of endometrial cancers (EC), plays an important role in the initiation and progression of many cancers. Inhibitors against various components of this pathway might promise a novel effective approach for targeted therapy for EC in the future. Intriguingly, two major members of this pathway, AKT1 and mTOR, were both reported to be the putative target genes of miR-99a, which were widely reported to function as a tumor suppressor in a variety of cancers. However, the direct role of miR-99a in endometrial cancer progression and the signaling pathways might been involved have never been deciphered. In this paper, we demonstrate that the expression of miR-99a was significantly suppressed in the EC tissues and was negatively correlated with the differentiation of tumors. Furthermore, we find that overexpression of miR-99a in EC cells induced a complex phenotype, namely an inhibition of cell proliferation, block of G1/S phase transition, induction of cell apoptosis, suppression of cell invasion, and inhibition of tumor growth in vivo, which was mediated, at least partially, through dual-suppression of PI3K/AKT/mTOR pathway. This finding not only helps us understand the molecular mechanism of endometrial carcinogenesis, but also gives us a strong rationale to further investigate miR-99a as a potential biomarker and therapeutic target for EC. 

Retracted: No

PubPeer comments:
 Similar mice in different tumor models! , 
 Another issue is the 2017 oncotarget paper used male mice as cervical cancer model which might be not appropriate. , 
 This paper has exact same style as another Chinese papers: STAT3 is involved in miR-124-mediated suppressive effects on esophageal cancer cells BMC Cancer (2015) - 0 Comments doi: 10.1186 s12885-015-1303-0 issn: 1471-2407 pubmed: 25928665 , 
 #3 *[right]* Figure 2C.  MiR-99a inhibits proliferation and invasion of EC cells. ... C, D. The influences of miR-99a on cell cycle distribution and apoptosis of HEC-1B and ishikawa cells were analyzed using fluorescence-activated cell sorting (FACS) . *[left]* Figure 3C from [Cheng et al (2015)] .  MiR-124 suppresses esophageal cancer cell growth. ...(C, D) The influences of miR-124 on cell apoptosis and cell cycle progression were analyzed using fluorescence-activated cell sorting (FACS) .  ,
LncRNA SNHG3 promotes the growth and metastasis of colorectal cancer by regulating miR-539/RUNX2 axis
Authors: Wen Dacheng
Liu Jingjing
Zhao Shutao
Zhu Jiaming
Li Songhe
Jiang Weidong
Journal: Biomedicine & Pharmacotherapy (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Colorectal cancer; RUNX2; SNHG3; miR-539.
Affiliations: Department of Gastrointestinal Nutrition and Hernia Surgery, the Second Hospital of Jilin University, Nanguan District, Changchun, 130041, China., Department of Ophthalmology, the First Hospital of Jilin University, Chaoyang District, Changchun, 130021, China. Electronic address: ., Department of Hepatobiliary and Pancreatic Surgery, the Second Hospital of Jilin University, Nanguan District, Changchun, 130041, 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 Authors and Editor-in-Chief. The corresponding author notified the journal that ‚ÄúLncRNA SNHG3 did not affect colorectal cancer cell invasion, which was inconsistent with our published results‚Ä? As the results were unreliable the authors requested its retraction. The journal was also alerted to suspected image similarities within Figure 2D, that appear to be present in another publication, as detailed here: https://pubpeer.com/publications/7855CA1A494A20F55AAE1463D1B648. The journal requested the authors provide an explanation and source data relating to the affected figure. The Authors did not provide an explanation in response to these concerns. The Editor-in-Chief assessed this case and decided to retract the article. 

Retracted: No

PubPeer comments:
 Fig 2D. Cell  invasion ... determined in **SW480** cells transfected with si-NC or **si-SNHG3**.  Fig 3B from [Yang et al (2020)] .  The cell invasion was determined in A549 and **SPC-A1** cells infected with sh-NC and **sh-LINC00525**.  Different cell-lines, treatments and scales. Same images. Can the authors of either paper comment? ,
Regulated Activating Thr172 Phosphorylation of Cyclin-Dependent Kinase 4(CDK4): Its Relationship with Cyclins and CDK ‚ÄúInhibitors‚Ä?1
Authors: Pierre P Roger
Katia Coulonval
Jacques E Dumont
Sabine Paternot
Yvan de Launoit
Laurence Bockstaele
Hugues Kooken
Frederick Libert
Journal: Molecular and Cellular Biology (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cyclin-dependent kinase 4; CDK4; Thr172 phosphorylation; D-type cyclins; Cip/Kip CDK inhibitors
Affiliations: Institute of Interdisciplinary Research, Universit√© Libre de Bruxelles, Campus Erasme, B-1070 Brussels, Belgium., Institute of Interdisciplinary Research, Department of Molecular Virology

Abstract:  Cyclin-dependent kinase 4 (CDK4) is a master integrator of mitogenic and antimitogenic extracellular signals. It is also crucial for many oncogenic transformation processes. Various molecular features of CDK4 activation remain poorly known or debated, including the regulation of its association with D-type cyclins, its activating Thr172 phosphorylation, and the roles of Cip/Kip CDK "inhibitors" in these processes. Thr172 phosphorylation of CDK4 was reinvestigated using two-dimensional gel electrophoresis in various experimental systems, including human fibroblasts, canine thyroid epithelial cells stimulated by thyrotropin, and transfected mammalian and insect cells. Thr172 phosphorylation of CDK4 depended on prior D-type cyclin binding, but Thr172 phosphorylation was also found in p16-bound CDK4. Opposite effects of p27 on cyclin D3-CDK4 activity observed in different systems depended on its stoichiometry in this complex. Thr172-phosphorylated CDK4 was enriched in complexes containing p21 or p27, even at inhibitory levels of p27 that precluded CDK4 activity. Deletion of the p27 nuclear localization signal sequence relocalized cyclin D3-CDK4 in the cytoplasm but did not affect CDK4 phosphorylation. Within cyclin D3 complexes, T-loop phosphorylation of CDK4, but not of CDK6, was directly regulated, identifying it as a determining target for cell cycle control by extracellular factors. Collectively, these unexpected observations indicate that CDK4-activating kinase(s) should be reconsidered. 

Retracted: No

PubPeer comments:
 Figure 7B. IP p27. Cyclin D3 panel does not look like it comes from the same blot as the CDK4, CDK6, CDK2, or p27 panels. All these proteins have similar molecular weights.  ,
EET agonist prevents adiposity and vascular dysfunction in rats fed a high fat diet via a decrease in Bach 1 and an increase in HO-1 levels
Authors: John R Falck
Nitin Puri
Komal Sodhi
Kazuyoshi Inoue
Michal L Schwartzman
Nader G Abraham
Journal: Prostaglandins & other lipid mediators (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: EETs; heme oxygenase; adipogenesis; obesity; cardio-metabolic dysfunction
Affiliations: Department of Physiology and Pharmacology, The University of Toledo College of Medicine, Health Education Building, 3000 Arlington Avenue, Toledo, OH 43614-2598, USA.

Abstract:  Recent reports have shown interplay between EETs (epoxides) and the heme oxygenase (HO) system in attenuating adipogenesis in cell culture models; prompting an examination of the effectiveness of EET agonist on obesity and associated cardio-metabolic dysfunction. Patho-physiological effects of an EET agonist (NUDSA) were contrasted in the absence and in the presence of stannous mesoporphyrin (an HO inhibitor) in SD rats fed a high fat (58%, HF) for 16 weeks. Animals on HF diet exhibited enhanced oxidative stress, increased levels of inflammatory cytokines and decreased levels of adiponectin along with reduced vascular and adipose tissue levels of EETs, HO-1; as compared to control rats (11% dietary fat). Treatment with NUDSA not only reversed serum adiponectin and vascular and adipose tissue levels of EETs and HO-1, but also, decreased blood pressure, subcutaneous and visceral fat content and serum TNFŒ± and IL-6 levels in rats on HF diet. Aortic endothelial function, peNOS expression and adipose tissue markers of energy homeostasis i.e. pAMPK, Sirt1 and FAS, impaired in rats fed a HF diet, were restored in animals treated with this EET agonist. That NUDSA enhanced HO-1 expression, was accompanied by increase in p-GSK-3Œ≤ and pAKT levels along with attenuation of adipose tissue levels of Bach 1--the transcriptional suppresser of HO-1 expression. Prevention of these beneficial effects of NUDSA, in animals on HF diet and concurrently exposed to NUDSA and SnMP, supports the role of EET-HO interaction in mediating such effects. Taken together, our findings suggest that the EETs stimulate HO-1 expression via suppression of Bach 1 and interplay of these two systems affords vascular and metabolic protection in diet induced obesity. 

Retracted: No

PubPeer comments:
 The lamin and actin panels are remarkably similar if one flips the actin panel bottom to top. Can the authors comment on this?    , 
 The same Western blot lanes identified in this paper as AKT show up in three other papers identified as actin. Would the authors care to comment? See also: https: pubpeer.com publications B3ABFE1EBACF517FD703E0BED6354F  , 
 In panel B of figure 6 (labeled  Nuclear Bach 1) and panel B of figure 7 (labelled  pAMPK ), the boxed lanes appear to be different exposures of the same blot, but rotated 180 degrees about the perpendicular axis in the case of pAMPK in figure 7B. Can the authors comment?   ,
Aqueous rechargeable zinc/sodium vanadate batteries with enhanced performance from simultaneous insertion of dual carriers
Authors: Xi Dai
Xinyu Wang
Fang Wan
Linlin Zhang
Zhiqiang Niu
Jun Chen
Journal: Nature Communications (2018)
Discipline: Multidisciplinary
Keywords: Rechargeable aqueous zinc-ion batteries; positive electrodes; energy storage mechanisms; zinc/sodium vanadate system; sodium vanadate hydrate nanobelts
Affiliations: Key Laboratory of Advanced Energy Materials Chemistry (Ministry of Education), College of Chemistry, Nankai University, Tianjin, 300071, P. R. China., Key Laboratory of Advanced Energy Materials Chemistry (Ministry of Education), College of Chemistry, Nankai University, Tianjin, 300071, P. R. China. ., Collaborative Innovation Center of Chemical Science and Engineering, Nankai University, Tianjin, 300071, P. R. China.

Abstract:  Rechargeable aqueous zinc-ion batteries are promising energy storage devices due to their high safety and low cost. However, they remain in their infancy because of the limited choice of positive electrodes with high capacity and satisfactory cycling performance. Furthermore, their energy storage mechanisms are not well established yet. Here we report a highly reversible zinc/sodium vanadate system, where sodium vanadate hydrate nanobelts serve as positive electrode and zinc sulfate aqueous solution with sodium sulfate additive is used as electrolyte. Different from conventional energy release/storage in zinc-ion batteries with only zinc-ion insertion/extraction, zinc/sodium vanadate hydrate batteries possess a simultaneous proton, and zinc-ion insertion/extraction process that is mainly responsible for their excellent performance, such as a high reversible capacity of 380 mAh g-1 and capacity retention of 82% over 1000 cycles. Moreover, the quasi-solid-state zinc/sodium vanadate hydrate battery is also a good candidate for flexible energy storage device. 

Retracted: No

PubPeer comments:
 Three groups of curves (an, ckl, fj) in Figure 5c are surprisingly identical.  , 
 We sincerely appreciate you for careful review. We have carefully checked the raw data. The raw data of the curves in these three groups is different. We find that this error is attributed to our carelessness of copying the data in the Origin and plotting them together. The curves at j, k, l, n have been corrected. The corrected figure is displayed as below. We feel very sorry for this mistake. The updated FTIR result in Figure 5c still supports the original conclusion. Thank you very much for pointing out this serious mistake, and we feel very sorry for our carelessness and any confusion caused. ,
MicroRNA-375 represses tumor angiogenesis and reverses resistance to sorafenib in hepatocarcinoma
Authors: Jian-Qiong Feng
Hua Li
Mao-Lin Shi
Tao Zhang
Yu-Di Bai
Yu Liu
Dong Li
Chao Wang
Jing-Jing Peng
Tao Wang
Dan Wang
Fei-Fan Sun
Journal: Cancer Gene Therapy (2021)
Discipline: CLINICAL MEDICINE
Keywords: Sorafenib; miRNAs; hepatocellular carcinoma; miR-375; PDGFC
Affiliations: Department of Oncology, The General Hospital of Western Theater Command PLA, Chengdu, 610083, Sichuan Province, China., Department of Pathology, The General Hospital of Western Theater Command PLA, Chengdu, 610083, Sichuan Province, China., Department of Oncology, The General Hospital of Western Theater Command PLA, Chengdu, 610083, Sichuan Province, China. .

Abstract:  Sorafenib was originally identified as an inhibitor of multiple oncogenic kinases and remains the first-line systemic therapy for advanced hepatocellular carcinoma (HCC). MicroRNAs (miRNAs) have been reported to play critical roles in the initiation, progression, and drug resistance of HCC. In this study, we aimed to identify sorafenib-induced miRNAs and demonstrate their regulatory roles. First, we identified that the expression of the tumor-suppressive miRNA miR-375 was significantly induced in hepatoma cells treated with sorafenib, and miR-375 could exert its antiangiogenic effect partially via platelet-derived growth factor C (PDGFC) inhibition. Then, we demonstrated that sorafenib inhibited PDGFC expression by inducing the expression of miR-375 and a transcription factor, achaete-scute homolog-1 (ASH1), mediated the induction of miR-375 by sorafeinb administration in hepatoma cells. Finally, we verified that the expression of miR-375 was reduced in sorafenib-resistant cells and that the restoration of miR-375 could resensitize sorafenib-resistant cells to sorafenib partially by the degradation of astrocyte elevated gene-1 (AEG-1). In conclusion, our data demonstrate that miR-375 is a critical determinant of HCC angiogenesis and sorafenib tolerance, revealing a novel miRNA-mediated mechanism underlying sorafenib treatment. 

Retracted: No

PubPeer comments:
 In Figure 3A, some of the tumors from two different experiments (Hep3b and Hepg2) share some similarities. They are not identical, but the shape of them are similar and they could have been turned around. I am surprised by the lack of variation in tumor size when comparing two different experiments. This is true for the experiments presented in both Figure 3A and Figure 6. In Figure 5H and F, a Western immunoblot panel are very similar.  , 
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Ginsenoside Rh2 induces DNA damage and autophagy in vestibular schwannoma is dependent of LAMP2 transcriptional suppression
Authors: Dong Yang
Xin Li
Xiaoyan Zhang
Journal: Biochemical and Biophysical Research Communications (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Autophagy; DNA damage; NR2F2; Rh2; VS.
Affiliations: Department of Otorhinolaryngology, Tianjin Medical University General Hospital, No.154 Anshan Road, Heping District, Tianjin, 300052, China., Department of Otorhinolaryngology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, No.168 Litang Road, Changping District, Beijing, 102218, China. Electronic address: ., Department of Allergy, The First Hospital of Qinhuangdao City, No.258 Cultural Road, Qinhuangdao, 066000, Hebei, China.

Abstract:  Ginsenoside Rh2 (G-Rh2), a component of ginseng extraction, exerted anti-tumor property in the occurrence and progress of human tumors. Vestibular schwannoma (VS) is a kind of benign tumor. Extraction of traditional Chinese herb has been applied to treat VS as adjuvant therapy. Nevertheless, G-Rh2-related molecular mechanisms in VS progress are not yet clear. The purpose of current study is to unveil the function and potential molecular mechanism of Rh2 in VS cellular functions. At first, the viability and apoptosis of VS cells treated with different concentrations of Rh2 were assessed. Autophagy and DNA damage response can be induced by multiple drugs. Here, we observed the changes of autophagy and DNA damage in Rh2-induced VS cells. Based on the experimental data, treatment with Rh2 contributed to cell apoptosis by inducing DNA damage and suppressing DNA damage. LAMP2 (lysosomal associated membrane protein 2), an autophagy inducer, was downregulated in Rh2-treated VS cells. Through mechanism study, we determined that Rh2 led to the transcriptional inactivation of LAMP2 by downregulating its transcription activator NR2F2 (nuclear receptor subfamily 2 group F member 2). In addition, NR2F2 overexpression recovered the role of Rh2 in cell functions, which was further rescued by the silence of LAMP2. Collectively, our study unveiled a novel NR2F2/LAMP2 axis in Rh2-mediated VS cells, which potentially contributes to the therapy for VS. 

Retracted: No

PubPeer comments:
 Concern about Figure 1B. The  30 and  40 panels appear to share similar groups of events (dots). Boxes of the same color highlight some of those regions. The panels are not identical, but more similar than expected. Could the authors please check?  ,
Precise therapeutic effect of self-assembling gold nanocluster‚ÄìPTEN complexes on an orthotropic model of liver cancer
Authors: Maonan Wang
Lishan Wang
Jiahua Zhou
Huan Feng
Xuemei Wang
Hui Jiang
Journal: Journal of Cancer Research and Clinical Oncology (2020)
Discipline: CLINICAL MEDICINE
Keywords: In situ; Liver cancer; Synthesized; The orthotropic liver tumor model; surgical orthotropic implantation.
Affiliations: State Key Laboratory of Bioelectronics (Chien-Shiung Wu Lab), School of Biological Science and Medical Engineering, Southeast University, Nanjing, 210096, China., Department of Hepatic-Biliary-Pancreatic Center, Zhongda Hospital, Southeast University, Nanjing, China., Department of Hepatobiliary Surgery Research Institute, Southeast University, Nanjing, China., Department of Hepatic-Biliary-Pancreatic Center, Zhongda Hospital, Southeast University, Nanjing, China. ., Department of Hepatobiliary Surgery Research Institute, Southeast University, Nanjing, China. ., State Key Laboratory of Bioelectronics (Chien-Shiung Wu Lab), School of Biological Science and Medical Engineering, Southeast University, Nanjing, 210096, China. .

Abstract:  Purpose: Presently, liver cancer is still one of the malignant tumors with high mortality. As far as the treatment of liver cancer is concerned, the most effective method is still liver transplantation. But every year, many liver cancer patients die from the lack of a proper liver transplant, or from waiting for a liver transplant. Therefore, it is very important to find new and effective treatment for patients with liver cancer. Methods: Herein, the cell model and the orthotropic liver tumor mice model have been performed to verify the results of our treatment. We found that the in situ synthesized gold nanocluster-PTEN (GNC-PTEN) complexes can effectively target and realize the fluorescence imaging of the liver tumor. Results: GNC-PTEN complexes could inhibit the proliferation, invasion, and metastasis of liver cancer cells. And the results also showed that GNC-PTEN complexes could be well targeted liver tumor at 6 h and the liver tumor in mice group treated with GNC-PTEN complexes almost disappeared. Conclusion: This is a simply and effectively method to realize liver cancer imaging and inhibition. This may raise the possibility for the accurate image/diagnosis and simultaneously efficient treatment of liver cancer in the relevant clinic application. 

Retracted: No

PubPeer comments:
 A couple of the mice displayed in Figure 2 seem to have been duplicated (however, not the fluorescence). There are also weird repeated elements in the abdominal region that can be seen in some panels. Perhaps easiest to see are the repeated artifacts in orange. Are these very consistent surgical scars? Could the authors double check their original images?  ,
The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6
Authors: Qian Wang
Xiangkai Meng
Yanan Wang
Yi Guo
Hong Shang
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: HPV16; E6; ING4; p53; acetylation
Affiliations: Department of Gynecology, First Affiliated Hospital of China Medical University, Shenyang, China.

Abstract:  High risk subtype HPV16 early oncoprotein E6 contributes host cell immortalization and transformation through interacting with a number of cellular factors. ING4 is one member of the inhibitor of growth (ING) family of type II tumor suppressors and it has been shown to be involved in regulating p53 function. However, the effect and mechanism of HPV16 E6 on ING4 function remain elusive. In this study, we report HPV16 E6 combines with ING4 in vivo and in vitro. The ING4 induced p53 acetylation and its combining with p53 were attenuated by HPV16 E6 independent of p53 degradation. The enhancing function of ING4 on p53 mediated apoptosis was diminished when HPV16 E6 existed. These findings reveal that ING4 may be a common target of oncogenic viruses for driving host cell carcinogenesis. 

Retracted: No

PubPeer comments:
 Figure 1. * Magenta arrows: Possible splices between lanes * Red boxes: Two ING bands in Figure 1B look similar to mirrored two lanes in the E6 panel in Figure 1C * The bottom panel in Figure 1C appears to show repeating patterns as shown with yellow circles, and unexpected blocks and lines in the right lane. * The bottom panel in Figure 1D shows an unexpected discontinuation in the second lane (green arrow) Reported to the journal in October 2015, but no action as of today.  ,
CXCL5 promotes the proliferation and migration of glioma cells in autocrine- and paracrine-dependent manners
Authors: Jun Wu
Quan Cheng
Fenghua Chen
Zhijie Dai
Ying Wang
Mingyu Zhang
Tao Song
Yong Guo
Journal: Oncology Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: CXCL5; CXCR2; tumorigenesis; cancer progression; glioma
Affiliations: Institute of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China., Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

Abstract:  CXCL5 and its receptor CXCR2 have been found to be involved in tumorigenesis and cancer progression. Recent studies have shown that CXCR2 is upregulated in glioma tissues, and associated with poor prognosis and recurrence. However, the role of CXCL5/CXCR2 signaling in mediating the malignant phenotypes of glioma cells, as well as the underlying mechanism, still remains unclear. In the present study, we found that CXCL5 was upregulated in glioma tissues compared to that noted in normal brain tissues. High CXCL5 levels were significantly associated with higher tumor grade, advanced clinical stage, and shorter survival time of glioma patients. In vitro studies indicated that the protein expression levels of CXCL5 and CXCR2 were markedly higher in human glioma cell lines (U87, U251, U373 and A172), when compared with those in normal human gliocyte HEB cells. Overexpression of CXLC5 significantly promoted the proliferation and migration of U87 cells, while knockdown of CXCL5 by small interfering RNA markedly inhibited U87 cell proliferation and migration. Moreover, both exogenous CXCL5 treatment and the conditioned medium of CXCL5-overexpressing HEB cells also enhanced the proliferation and migration of U87 cells. Molecular mechanism investigation revealed that CXLC5 activated the ERK, JNK, p38 MAPK signaling pathways, which play key roles in tumor growth and metastasis. According to these data, our study suggests that CXCL5 plays a promoting role in glioma in autocrine- and paracrine-dependent manners. 

Retracted: Yes

PubPeer comments:
 Figures 1 and 2 show stomachs of rats treated with different compounds and concentrations. However some panels representing different treatments appear to look similar. * Red boxes: RIS-0.03 in Figure 1 looks similar to KET-10 in Figure 2, albeit rotated 180 degrees * Green boxes: RIS-0.3 in Figure 1 looks similar to RIS-0.1 in Figure 2, albeit rotated 90 degrees * Blue boxes: RIS-1.0 in Figure 1 looks similar to KET-10 in Figure 1, albeit slightly rotated and stretched  ,
MicroRNA-150 aggravates H2O2-induced cardiac myocyte injury by down-regulating c-myb gene
Authors: Qunjun Duan
Aiqiang Dong
Xuebiao Li
Minjian Kong
Daming Jiang
Jianfang Qian
Journal: Acta biochimica et biophysica Sinica (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: cardiac myocyte apoptosis; cell death; microRNA; reactive oxygen species.
Affiliations: Department of Cardiothoracic Surgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Abstract:  MicroRNAs (miRNAs) are one class of non-coding RNAs that play an important role in post-transcriptional regulation via the degradation or translational inhibition of their target genes. MicroRNA-150 (miR-150) plays a vital role in regulating the development of B and T lymphocytes. Although the dysregulation of miR-150 was confirmed in human myocardial infarction, little is known regarding the biological functions of miR-150 in response to reactive oxygen species (ROS)-mediated gene regulation in cardiac myocytes. Using quantitative real-time reverse transcription-polymerase chain reaction, we demonstrated that the level of miR-150 was up-regulated in cardiac myocytes after treatment with hydrogen peroxide (H2O2). To identify the potential roles of miR-150 in H2O2-mediated gene regulation, we modulated expression of miR-150 using miR-150 inhibitor and miR-150 mimics. Results showed that silencing expression of miR-150 decreased H2O2-induced cardiac cell death and apoptosis. In lymphocytes, c-myb was a direct target of miR-150. In cardiac myocytes, we found that c-myb was also involved in miR-150-mediated H2O2-induced cardiac cell death. These results suggested that miR-150 participates in H2O2-mediated gene regulation and functional modulation in cardiac myocytes. MiR-150 may play an essential role in heart diseases related to ROS, such as cardiac hypertrophy, heart failure, myocardial infarction, and myocardial ischemia/reperfusion injury. 

Retracted: No

PubPeer comments:
 The authors of this paper coined a new notion for multiple attribute decision making called u201c**spherical linguistic numbers**u201d. A spherical linguistic number contains two parts, a linguistic term and a triplet called spherical fuzzy number (See Definition 2). Some operations are defined in Definition 3 for spherical linguistic numbers. However, some operations make no sense. A concrete example is illustrated on https: pubpeer.com publications 3BF9D24A1ACA22AE922123950660A6 A theory based on such notions and operations is merely symbol manipulation.   ,