PReD-Bench/PRed-Bench huggingface dataset:
RETRACTED: One isoform of Arg/Abl2 tyrosine kinase is nuclear and the other seven cytosolic isoforms differently modulate cell morphology, motility and the cytoskeleton
Authors: Cristina Bianchi
Vitalba Di Stefano
Silvia Bombelli
Rita Facchetti
Roberto A Perego
Barbara Torsello
Maria A Zipeto
Journal: Experimental Cell Research (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Abelson related gene; Arg; Cell morphology; Cell motility; Cytoskeleton
Affiliations: Department of Health Sciences, Milano-Bicocca University, 20900 Monza (MB), Italy., Department of Health Sciences, Milano-Bicocca University, 20900 Monza (MB), Italy. Electronic address: .

Abstract:  The non-receptor tyrosine kinase Abelson related gene (Arg/Abl2) regulates cell migration and morphogenesis by modulating the cytoskeleton. Arg promotes actin-based cell protrusions and spreading, and inhibits cell migration by attenuating stress fiber formation and contractility via activation of the RhoA inhibitor, p190RhoGAP, and by regulating focal adhesion dynamics also via CrkII phosphorylation. Eight full-length Arg isoforms with different N- and C-termini are endogenously expressed in human cells. In this paper, the eight Arg isoforms, subcloned in the pFLAG-CMV2 vector, were transfected in COS-7 cells in order to study their subcellular distribution and role in cell morphology, migration and cytoskeletal modulation. The transfected 1BSCTS Arg isoform has a nuclear distribution and phosphorylates CrkII in the nucleus, whilst the other isoforms are detected in the cytoplasm. The 1BLCTL, 1BSCTL, 1ASCTS isoforms were able to significantly decrease stress fibers, induce cell shrinkage and filopodia-like protrusions with a significant increase in p190RhoGAP phosphorylation. In contrast, 1ALCTL, 1ALCTS, 1ASCTL and 1BLCTS isoforms do not significantly decrease stress fibers and induce the formation of retraction tail-like protrusions. The 1BLCTL and 1ALCTL isoforms have different effects on cell migration and focal adhesions. All these data may open new perspectives to study the mechanisms of cell invasiveness. 

Retracted: Yes

PubPeer comments:
 I have concerns about Figure 3A. Blue boxes indicates a set of bands that appear unexpectedly similar; red boxes indicate a set of bands that appear very similar if one is flipped horizontally and vertically. I did not look elsewhere in this paper. Similar issues for papers with shared co-authors: https: pubpeer.com publications 7338E21D16FA9AF67322800CEDC0D9 https: pubpeer.com publications 159D21A5FEE9E11C837DEE235CA2F0#6 *** ![file] *** ![file] , 
 2020 retraction. https: www.sciencedirect.com science article pii S0014482720302706?via%3Dihub This article has been retracted at the request of the Editor in Chief. The image analyses run on Western blots in Fig 1D and 3A strongly suggested inappropriate image manipulations. Upon request, the authors neither provided the original data nor a satisfactory explanation. Manipulating images in any part of a publication is ethically not acceptable. ,
Effect of N-Acetylserotonin on Intestinal Recovery Following Intestinal Ischemia–Reperfusion Injury in a Rat
Authors: Yoav Ben Shahar
Nir Bitterman
Arnold Coran
Dmitriy Chepurov
Arie Bitterman
Igor Sukhotnik
Jacob Bejar
Yulia Pollak
Journal: European Journal of Pediatric Surgery (2015)
Discipline: CLINICAL MEDICINE
Keywords: N-acetylserotonin; intestinal recovery; enterocyte turnover; ischemia-reperfusion; gut mucosal damage
Affiliations: Laboratory of Intestinal Adaptation and Recovery, The Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel, Department of Pathology, Bnai Zion Medical Center, Haifa, Israel, Section of Pediatric Surgery, C.S. Mott Children's Hospital, University of Michigan Medical School, Ann Arbor, Michigan, United States, Department of Surgery, Carmel Medical Center, Haifa, Israel, Department of Pediatric Surgery, Bnai Zion Medical Center, Haifa, Israel

Abstract:  Objective: N-acetylserotonin (NAS) is a naturally occurring chemical intermediate in the biosynthesis of melatonin. Extensive studies in various experimental models have established that treatment with NAS significantly protects heart and kidney injury from ischemia-reperfusion (IR). The purpose of the present study was to examine the effect of NAS on intestinal recovery and enterocyte turnover after intestinal IR injury in rats. Methods: Male Sprague-Dawley rats were divided into four experimental groups: (1) Sham rats underwent laparotomy, (2) sham-NAS rats underwent laparotomy and were treated with intraperitoneal (IP) NAS (20 mg/kg); (3) IR rats underwent occlusion of both superior mesenteric artery and portal vein for 30 minutes, followed by 48 hours of reperfusion, and (4) IR-NAS rats underwent IR and were treated with IP NAS (20 mg/kg) immediately before abdominal closure. Intestinal structural changes, Park injury score, enterocyte proliferation, and enterocyte apoptosis were determined 24 hours following IR. The expression of Bax, Bcl-2, p-ERK, and caspase-3 in the intestinal mucosa was determined using real-time polymerase chain reaction, Western blot, and immunohistochemistry. A nonparametric Kruskal-Wallis analysis of variance test was used for statistical analysis with p less than 0.05 considered statistically significant. Results: Treatment with NAS resulted in a significant increase in mucosal weight in jejunum and ileum, villus height in the ileum, and crypt depth in jejunum and ileum compared with IR animals. IR-NAS rats also had a significantly proliferation rates as well as a lower apoptotic index in jejunum and ileum which was accompanied by higher Bcl-2 levels compared with IR animals. Conclusions: Treatment with NAS prevents gut mucosal damage and inhibits programmed cell death following intestinal IR in a rat. 

Retracted: No

PubPeer comments:
 Could the authors check the pU and pU2 columns in Fig 4A? I suppose it is possible that an additional 24 hours of incubation in culture solution flipped the former spheroid aggregate combination horizontally, and made no difference at all to the latter combination, but it seems more likely that an error occurred during figure assembly. ![file] ,
Deficient spermiogenesis in mice lacking Rlim
Authors: Jesse Mager
Ana Bošković
Darya A Tourzani
Fengyun Sun
Feng Wang
Maria Gracia Gervasi
Pablo E Visconti
Lihua Julie Zhu
Oliver J Rando
Lara Strittmatter
Jun Yu
Vera D Rinaldi
Ingolf Bach
Mary C Wallingford
Journal: eLife (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Rlim; cytoplasmic reduction; developmental biology; mouse; mouse genetics
Affiliations: Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, United States., Department of Veterinary & Animal Sciences, University of Massachusetts Amherst, Amherst, United States., Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, United States., Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, United States., Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, United States., Electron Microscopy Core, University of Massachusetts Medical School, Worcester, United States.

Abstract:  The X-linked gene Rlim plays major roles in female mouse development and reproduction, where it is crucial for the maintenance of imprinted X chromosome inactivation in extraembryonic tissues of embryos. However, while females carrying a systemic Rlim knockout (KO) die around implantation, male Rlim KO mice appear healthy and are fertile. Here, we report an important role for Rlim in testis where it is highly expressed in post-meiotic round spermatids as well as in Sertoli cells. Systemic deletion of the Rlim gene results in lower numbers of mature sperm that contains excess cytoplasm, leading to decreased sperm motility and in vitro fertilization rates. Targeting the conditional Rlim cKO specifically to the spermatogenic cell lineage largely recapitulates this phenotype. These results reveal functions of Rlim in male reproduction specifically in round spermatids during spermiogenesis. 

Retracted: No

PubPeer comments:
 Throughout Fig. 7 (panels BCDF) the authors appear to use a two-factor design in which testis weight is compared between two different conditional KO mice and their littermates. I believe that the authors should therefore verify that the KO-littermate differences are actually different between the two KOs. This is not done:  the difference between significant and non-significant is non-significant ... In the present case, the conclusions probably won t be altered, except maybe in panel 7B, but the p-values may become larger. ![image] The  Transparent reporting form says:  Statistical results are shown in Figures. Statistical analyses methods are indicated in the Figure Legends and or in the Materials and methods section.  However, I was unable to find any mention of the statistical tests applied, although they are presumably simple t-tests. ,
Rosiglitazone, an Agonist of PPARgamma, Inhibits Non-Small Cell Carcinoma Cell Proliferation In Part through Activation of Tumor Sclerosis Complex-2
Authors: Jesse Roman
Ying Zheng
Shouwei Han
Journal: PPAR research (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: PPARgamma ligands; non-small cell lung carcinoma; NSCLC; proliferation; mTOR pathway
Affiliations: Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Emory University School of Medicine, Emory University, Atlanta, GA 30322, USA.

Abstract:  PPARgamma ligands inhibit the proliferation of non-small cell lung carcinoma (NSCLC) cells in vitro. The mechanisms responsible for this effect remain incompletely elucidated, but PPARgamma ligands appear to inhibit the mammalian target of rapamycin (mTOR) pathway. We set out to test the hypothesis that PPARgamma ligands activate tuberous sclerosis complex-2 (TSC2), a tumor suppressor gene that inhibits mTOR signaling. We found that the PPARgamma ligand rosiglitazone stimulated the phosphorylation of TSC2 at serine-1254, but not threonine-1462. However, an antagonist of PPARgamma and PPARgamma siRNA did not inhibit these effects. Rosiglitazone also increased the phosphorylation of p38 MAPK, but inhibitors of p38 MAPK and its downstream signal MK2 had no effect on rosiglitazone-induced activation of TSC2. Activation of TSC2 resulted in downregulation of phosphorylated p70S6K, a downstream target of mTOR. A TSC2 siRNA induced p70S6K phosphorylation at baseline and inhibited p70S6K downregulation by rosiglitazone. When compared to a control siRNA in a thymidine incorporation assay, the TSC2 siRNA reduced the growth inhibitory effect of rosiglitazone by fifty percent. These observations suggest that rosiglitazone inhibits NSCLC growth partially through phosphorylation of TSC2 via PPARgamma-independent pathways. 

Retracted: No

PubPeer comments:
 Figure 3(b). Vertical change in background p-p70s6K panel, but not in other 2 panels. https: imgur.com WMwN5hl ,
Influence of anticoagulants on the measurement of S100B protein in blood
Authors: Luis V C Portela
Marcelo O Dietrich
Carlos A Gonçalves
Diogo O Souza
Adriano B L Tort
Journal: Clinical biochemistry (2003)
Discipline: CLINICAL MEDICINE
Keywords: anticoagulants; blood S100B levels; EDTA; heparin; citrate
Affiliations: Departamento de Bioquímica, ICBS, UFRGS, Brazil.

Abstract:  Objective: Evaluate anticoagulants influence on blood S100B levels. Design and methods: Blood from 18 healthy adult subjects were collected using: no anticoagulants; EDTA; heparin; and citrate. S100B levels were determined using LIA-mat assay. Results: Heparin and citrate increased S100B levels (p&lt;0.001), whereas EDTA had no effect (p=0.24). Heparin samples were highly (r2=0.97, p&lt;0.001), citrate samples were moderately (r2=0.49, p&lt;0.001), and EDTA samples were not (r2=0.22, p=0.059) correlated with serum samples. Conclusion: When anticoagulant is required, heparin should be the primary choice. 

Retracted: No

PubPeer comments:
 The value 93.00 is wrong, probably the correct one is 9, so it can be 29% of 31.00 ![file] ,
RETRACTED: A Societal Sleep Prescription
Authors: Matthew P Walker
Journal: Neuron (2019)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: global sleep-loss epidemic; health consequences; societal fabric; insufficient sleep; prescriptive remedies
Affiliations: Center for Human Sleep Science, Department of Psychology, University of California, Berkeley, CA 94720, USA; Helen Wills Neuroscience Institute, University of California, Berkeley, CA, USA. Electronic address: .

Abstract:  We are suffering a global sleep-loss epidemic. The health consequences within an individual are well characterized. But does society suffer just as much? Here, I discuss how insufficient sleep erodes our societal fabric as much as it does our biological fabric, and offer some prescriptive remedies. 

Retracted: Yes

PubPeer comments:
 2020 retraction. https: www.sciencedirect.com science article pii S0896627320305201?via%3Dihub This article has been retracted at the request of the Author. It has come to the authoru2019s attention that the degree of overlap between the contents of the NeuroView that he wrote for Neuron (Neuron 103 (2019) 559u2013562, https: doi.org 10.1016 j.neuron.2019.06.015) and a brief article that he had previously written for The Lancet (Lancet 391 (2018) 2598u20132599, https: doi.org 10.1016 S0140-6736(18)31316-3) is not acceptable according to Neuronu2019s policy. The 2018 piece focused on medicine, on the effect of lack of sleep on doctors and patients, while the 2019 piece discussed this as well as other effects on society, businesses, and children. Because of the reuse of several verbatim paragraphs, the Neuron article must be retracted, given Neuronu2019s instructions for authors and his disclosure at the time of publication. Apologies are offered to readers of the journal that this was not detected during the submission process. , 
 Here is a comparison of the The Lancet 2018 article (left) and the second half of the Neuron 2019 article (right), with colored blocks showing verbatim text identities between the two articles. Generated using SimilarityTexter, available at https: people.f4.htw-berlin.de ~weberwu simtexter app.html ![file] ![file] ![file] ,
miR‑885‑5p upregulation promotes colorectal cancer cell proliferation and migration by targeting suppressor of cytokine signaling
Authors: Fang Liu
Meng Su
Rui Zhang
Baoli Qin
Yuze Chen
Journal: Oncology Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: cell migration; cell proliferation; colorectal cancer; miR-885-5p; suppressor of cytokine signaling.
Affiliations: Department of Medical Oncology, Liaoning Cancer Hospital and Institute, Cancer Hospital of China Medical University, Shenyang, Liaoning 110042, P.R. China., Department of Colorectal Surgery, Liaoning Cancer Hospital and Institute, Cancer Hospital of China Medical University, Shenyang, Liaoning 110042, P.R. China.

Abstract:  The aim of the present study was to investigate the role of microRNA (miR)-885-5p in colorectal cancer cell proliferation and migration, and to determine the possible underlying molecular mechanisms. The expression of miR-885-5p in colorectal cancer tissue and cells was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expression levels of three suppressor of cytokine signaling (SOCS) factors were detected by RT-qPCR and western blotting. The effects of miR-885-5p on tumor cell proliferation and migration were studied using MTT and Transwell assays, respectively. Additionally, the expression levels of epithelial-mesenchymal transition (EMT)-related proteins (N-cadherin, E-cadherin, vimentin and Snail) were detected by RT-qPCR and western blot analysis. Furthermore, the target of miR-885-5p was predicted and confirmed using a luciferase reporter assay. miR-885-5p was demonstrated to be upregulated and SOCS was downregulated in colorectal cancer tissue, and cells. miR-885-5p suppression significantly inhibited tumor cell proliferation and migration, promoted E-cadherin expression, and inhibited the expression levels of N-cadherin, vimentin and Snail. Further studies showed that SOCS5, SOCS6 and SOCS7 were direct targets of miR-885-5p. The results suggest that miR-885-5p suppression inhibited cell proliferation and migration, and the EMT process by targeting SOCS5, SOCS6 and SOCS7 genes in colorectal cancer. miR-885-5p and SOCS may be used for the diagnosis and treatment of colorectal cancer. 

Retracted: No

PubPeer comments:
 Figure 3. * Red boxes: Two CAF2-1 panels appear to look very similar * Yellow boxes: Two Delta E4.2 panels appear to look partially similar ![file] ,
LncRNA SNHG19 Promotes the Development of Non-Small Cell Lung Cancer via Mediating miR-137/E2F7 Axis
Authors: Rui Wang
Guang-Yin Zhao
Zhao-Feng Ning
Journal: Frontiers in Oncology (2021)
Discipline: CLINICAL MEDICINE
Keywords: E2F7; MiR-137; long non-coding RNA (LncRNA) SNHG19; non-small cell lung cancer (NSCLC); tumorigenesis.
Affiliations: Department of Thoracic Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China., Radiotherapy Branch, Cancer Hospital, Taian, China., Department of Thoracic Surgery, The Third Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Abstract:  Objective: Non-small cell lung cancer (NSCLC) is a common malignant tumor, which has high incidence and low the 5-year survival rate. Long non-coding RNAs (lncRNAs) play critical roles in carcinoma occurrence and metastasis. Herein, our aim was to investigate the effects of lncRNA SNHG19 in NSCLC progression. Materials and methods: Long non-coding RNA Small Nucleolar RNA Host Gene 19 (lncRNA SNHG19) expression level was measured by bioinformatics and qRT-PCR. Edu, Transwell, and scratch assays were performed to explore the role of si-SNHG19 or SNHG19 on NSCLC progression. Luciferase assay was used to verify the relationship between SNHG19/E2F7 and miR-137. The experiment of Xenograft was used for exploring the function of SNHG19 in vivo. Results: SNHG19 was upregulated in cancer tissues, patients plasma and cell lines of NSCLC. Knockdown of SNHG19 inhibited cell proliferation, migration, and invasion. Luciferase assay confirmed that SNHG19 regulated E2F7 expression via interacting with miR-137. Overexpression of SNHG19 accelerated NSCLC tumor progression via miR-137/E2F7 axis both in vitro and in vivo. Conclusions: Our results clarified the SNHG19 function for the first time, and SNHG19 promoted the progression of NSCLC, which was mediated by the miR-137/E2F7 axis. This study might provide new understanding and targets for NSCLC diagnosis and treatment. 

Retracted: Yes

PubPeer comments:
 Figure 8 u2013 more similar than expected. Could authors check it please? ![file] ,
Downstream effectors of oncogenic ras in multiple myeloma cells
Authors: Brian Van Ness
Jung-hsin Hsu
Liping Hu
Alan Lichtenstein
Joseph Gera
Yijiang Shi
Journal: Blood (2003)
Discipline: CLINICAL MEDICINE
Keywords: Oncogenic ras; IL-6-independent growth; Signaling pathways; Mutated K-ras; Mutated N-ras
Affiliations: Hematology-Oncology Division, West Los Angeles Veteran's Administration-University of California Los Angeles Medical Center, Los Angeles, CA 90073, USA., From the Hematology-Oncology Division of the West Los Angeles Veteran's Administration-University of California Los Angeles Medical Center, Los Angeles, CA; and the Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN.

Abstract:  Ectopic expression of mutated K-ras or N-ras in the interleukin 6 (IL-6)-dependent ANBL6 multiple myeloma cell line induces cytokine-independent growth. To investigate the signaling pathways activated by oncogenic ras that may stimulate IL-6-independent growth, we compared ANBL6 cells stably transfected with mutated K or N-ras genes with wild-type ras-expressing control cells identically transfected with an empty vector. Upon depletion of IL-6, both mutated ras-containing myeloma lines demonstrated constitutive activation of mitogen-activated extracellular kinase 2(MEK)/extracellular signal-regulated kinase (ERK), phosphatidylinositol-3 kinase (PI3-kinase)/AKT, mammalian target of rapamycin (mTOR)/p70S6-kinase, and nuclear factor kappa B (NF-kappa B) pathways. In contrast, signal transducer and activator of transcription-3 (STAT-3) was not constitutively tyrosine phosphorylated in mutant ras-expressing cells. We used several maneuvers in attempts to selectively target these constitutively active pathways. The mTOR inhibitors rapamycin and CCI-779, the PI3-kinase inhibitor LY294002, and the MEK inhibitor PD98059 all significantly curtailed growth of mutant ras-containing cells. Farnesyl transferase inhibitors, used to target ras itself, had modest effects only against mutant N-ras-containing cells. Growth of mutant N-ras-containing myeloma cells was also inhibited by acute expression of the IKB superrepressor gene, which abrogated NF-kappa B activation. These results indicate that several pathways contributing to stimulation of cytokine-independent growth are activated downstream of oncogenic ras in myeloma cells. They also suggest that therapeutic strategies that target these pathways may be particularly efficacious in patients whose myeloma clones contain ras mutations. 

Retracted: No

PubPeer comments:
 Figure 3C u2013 more similar than expected ![file] Figure 4 u2013 more similar than expected ![file] ,
BRAF mutations in non-Hodgkin's lymphoma
Authors: S H Kim
S H Lee
W S Park
H S Kim
C J Kim
Y G Cho
J H Lee
N J Yoo
J Y Lee
S W Nam
Y H Soung
J Y Park
J W Lee
Y H Ko
S Y Kim
Journal: British Journal of Cancer (2003)
Discipline: CLINICAL MEDICINE
Keywords: Ras proteins; signalling pathways; cell growth; malignant transformation; BRAF
Affiliations: Department of Pathology, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Socho-gu, Seoul 137-701, Korea.

Abstract:  Ras proteins control signalling pathways that are key regulators of several aspects of normal cell growth and malignant transformation. BRAF, which encodes an RAF family member in the downstream pathway of RAS, is somatically mutated in a number of human cancers. The activating mutation of BRAF is known to play a role in tumour development. As there have been no data on the BRAF mutation in non-Hodgkin's lymphoma (NHL), we analysed the genomic DNAs from 164 NHLs by polymerase chain reaction (PCR)-based single-strand conformation polymorphism (SSCP) for the detection of somatic mutations of BRAF (exons 11 and 15). Overall, we detected BRAF mutations in four NHLs (2.4%). Whereas most BRAF mutations in human cancers involved V599 of BRAF, all of the four BRAF mutations in the NHLs involved other amino acids (one G468A, two G468R and one D593G). To our knowledge, this is the first report on BRAF mutation in NHL, and the data indicate that BRAF is occasionally mutated in NHL, and suggest that BRAF mutation may contribute to the tumour development in some NHLs. 

Retracted: No

PubPeer comments:
 Figure S5: more similar than expected. Could authors check please? ![file] ,
MiR-505 suppressed the growth of hepatocellular carcinoma cells via targeting IGF-1R
Authors: Yongshan Yao
Liang Ren
Shengqiang Wang
Yang Wang
Journal: Bioscience Reports (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: AKT; GLUT1; Hepatocellular carcinoma; IGF-1R; glycolysis
Affiliations: Department of Ultrasound and Imaging, Yichang Yiling Hospital, Yichang city 443100, Hubei province, China., Emergency and Trauma Surgery, The First College of Clinical Medical Science, China Three Gorges University, Yichang city 443100, Hubei province, China., Department of Pediatrics, Yichang Yiling Hospital, No.32 of Dong Hu street, Yiling district, Yichang city 443100, Hubei province, China .

Abstract:  Hepatocellular carcinoma (HCC) is one of the most common cancers globally. An increasing body of evidence has demonstrated the critical function of microRNAs (miRNAs) in the initiation and progression of human cancers. Here, we showed that miR-505 was down-regulated in HCC tissues and cell lines. Reduced expression of miR-505 was significantly correlated with the worse prognosis of HCC patients. Overexpression of miR-505 suppressed the proliferation, colony formation and induced apoptosis of both HepG2 and Huh7 cells. Further mechanism study uncovered that miR-505 bound the 3'-untranslated region (3'-UTR) of the insulin growth factor receptor (IGF-1R) and inhibited the expression of IGF-1R in HCC cells. The down-regulation of IGF-1R by miR-505 further suppressed the phosphorylation of AKT at the amino acid S473. Consistently, the abundance of glucose transporter (GLUT) 1 (GLUT1) was reduced with the overexpression of miR-505. Down-regulation of GLUT1 by miR-505 consequently attenuated the glucose uptake, lactate production and ATP generation of HCC cells. Collectively, our results demonstrated the tumor suppressive function of miR-505 possibly via inhibiting the glycolysis of HCC cells. These findings suggested miR-505 as an interesting target for designing anti-cancer strategy in HCC. 

Retracted: No

PubPeer comments:
 Fig 2E.  FACS analysis showed that the cell apoptosis percentage of HCC cells expressing miR-505 was higher than that of the control group . ![file] Each panel contains a halo of regularly-spaced dots, surrounding a central clump with a curious appearance, woven or crocheted in texture (also visible in [Zhao et al 2020] and [Qu et al 2020] ). Perhaps these are instrumentation artefacts of some kind. Is it possible for the authors to upload the raw data files to a data repository somewhere? ------------------------------------- Here is a spreadsheet containing similar examples of these crocheted beetroot scatterplots (currently 11 retractions): https: docs.google.com spreadsheets d 1NKBplrpW1txuL9PjhYb3bbvtQbk-TcsnqyqI8Uj-5Q8 edit?usp=sharing ,
Long noncoding RNA TP73-AS1 promotes non-small cell lung cancer progression by competitively sponging miR-449a/EZH2
Authors: Fengqi Fang
Lin Zhang
Xin He
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: EZH2; Non-small cell lung cancer; TP73-AS1; ceRNA; miR-449a.
Affiliations: Department of Respiratory Medicine, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China., Department of Respiratory Medicine, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. Electronic address: .

Abstract:  Long noncoding RNAs (lncRNAs) are a type of noncoding RNA transcript that are characterized by lack of protein-coding capacity. The vital role of lncRNAs in non-small cell lung cancer (NSCLC) is attracting increasingly more attention. In the present study, we investigate the role of lncRNA antisense RNA of the TP73 gene (TP73-AS1) in NSCLC carcinogenesis. The results demonstrate that TP73-AS1 is markedly upregulated in NSCLC tissues, and functional experiments revealed that TP73-AS1 is significantly increased in NSCLC tissue and cell lines, indicating a possible oncogenic role. In loss-of-function assays, the knockdown of TP73-AS1 inhibited NSCLC cell proliferation, tumor growth and cycle progression in vivo and in vitro. Bioinformatic tools predicted that miR-449a both targeted the 3'-UTR of TP73-AS1 and EZH2, which was confirmed using luciferase reporter assay and AGO2-dependent RNA immunoprecipitate (RIP). TP73-AS1 and miR-449a were in the same RNA-induced silencing complex (RISC). In summary, the results indicate an explicit oncogenic role of TP73-AS1 in the NSCLC tumorigenesis, suggesting a TP73-AS1-miR-449a-EZH2 axis and providing new insight for NSCLC tumorigenesis. 

Retracted: No

PubPeer comments:
  From **2016 to 2017**, a total of 45 lung cancer patients, who qualified as NSCLC by pathological diagnosis, were recruited at the First Affiliated Hospital of Dalian Medical University . Fig 1D.  Overall survival rate of NSCLC patients who had high or low TP73-AS1 levels. ![file] When this paper was submitted to the journal on 10 April 2018, survival of patients had been followed for 5 years after recruitment, i.e. through to the period **2021 to 2022**. ,
TRAF3 delays cyst formation induced by NF-κB signaling
Authors: Chaofeng Hu
Xinzhou Zhang
Liping Sun
Journal: IUBMB life (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Bcl-2; Bcl-xl; NF-κB; TRAF3; cyst formation.
Affiliations: Department of Nephrology; Shenzhen People's Hospital, Second Clinical Medical College, Jinan University; Shenzhen China, Department of Pathophysiology, School of Medicine; Jinan University; Guangzhou China

Abstract:  This study aims to investigate the effects of TNF receptors associated factor 3 (TRAF3) on the signaling pathway and expression of downstream products of nuclear factor kappa B (NF-κB) in the epithelial cells of renal ducts in individuals with polycystic kidney disease (PKD). We observe the TRAF3 genic overexpression of the epithelial cells, which form a tubular branch structure, in polycystic kidneys and to explore the protective effect of TRAF3 on the cystogenesis and progression of PKD. Western blotting analysis was conducted to examine the signaling changes of NF-κB in PKD the epithelial cells and TRAF3 transgenic PKD epithelial cells. Changes in the downstream apoptosis factor and cell proliferation in PKD epithelial cells and TRAF3 transgenic PKD epithelial cells were detected. A three-dimensional matrigel culture experiment was performed to examine abnormal tubulomorphogenesis in vitro. The overexpression of TRAF3 significantly inhibited the signaling pathway of NF-κB in the PKD epithelial cells, downregulated the expression of downstream factors Bcl-2 and Bcl-xl, and significantly decreased cystic epithelial cell proliferation. Additional branch structures were observed in the PKD epithelial cells with a three-dimensional culture compared to wildtype cells. TRAF3 may likely induce apoptosis and resistance to proliferation and may be a new target to inhibit the cyst formation in PKD by regulating the NF-κB signaling pathway Bcl-2 and Bcl-xl activity. © 2017 IUBMB Life, 69(3):170-178, 2017. 

Retracted: No

PubPeer comments:
 Figure 3. The IMCD and PKD epithelial cell actin panels appear to look unexpectedly similar. Shown with red boxes. ![file] , 
 Figure 4. The first two lanes of the p-IkBa and Bcl-2 panels look unexpectedly similar. Shown with blue boxes. ![file] , 
 Figure 7. Panels C ( TRAF3 overexpressed PKD renal collecting duct epithilial cell ) and D ( TRAF3 overex- pressed PKD renal collecting duct epithilial cell transfected with TRAF3 siRNA ) appear to share some similarities. Shown in scarlet red and metallic gold. ![file] , 
 Figure 7E. Some bands appear to look similar to each other. Arrows of the same color highlight bands that look similar. ![file] ,
Panepoxydone targets NF-kB and FOXM1 to inhibit proliferation, induce apoptosis and reverse epithelial to mesenchymal transition in breast cancer
Authors: Ming Tan
Steven McClellan
Windy Dean-Colomb
Clayton Yates
Yaguang Xi
Ritu Arora
Laurie B Owen
Bernard D Gary
Eddie Reed
Gary A Piazza
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Triple-negative breast cancer; NF-κB; panepoxydone; breast cancer cell lines; antitumor activity
Affiliations: Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, United States of America., Department of Biology and Center for Cancer Research, Tuskegee University, Tuskegee, Alabama, United States of America.

Abstract:  Background: Triple-negative breast cancer (TNBC) is a highly diverse group that is associated with an aggressive phenotype. Its treatment has been challenging due to its heterogeneity and absence of well-defined molecular targets. Thus, there is an urgent need to identify novel agents with therapeutic application. NF-κB is over-expressed in many breast cancers; thus, inactivation of the NF-κB pathway could serve as a therapeutic target. Here we report for the first time the anti-tumor activity of panepoxydone (PP), a NF-κB inhibitor isolated from an edible mushroom, in several breast cancer cell lines. Methods: We investigated the effects of PP on cell growth, migration-invasion, apoptosis and EMT-related proteins expression in MCF-7 and TNBC cell lines MDA-MB-231, MDA-MB-468 and MDA-MB-453. Results: Significant antitumor activity was seen in all cell lines, with differential responses noted in cell-line specific manner. Treatment with PP resulted in significant cytotoxicity, decreased invasion, migration and increased apoptosis in all cell lines tested. Up-regulation of Bax and cleaved PARP and down-regulation of Bcl-2, survivin, cyclin D1 and caspase 3 were noted in PP-treated breast cancer cells. The antitumor effect of PP appeared related to its ability to inhibit the phosphorylation of inhibitor of NF-κB (IκBα) with cytoplasmic accumulation. PP treatment also down-regulated FOXM1 which resulted in a reversal of EMT. Similar results were obtained after silencing of NF-kB and FOXM1. Conclusion: Altogether, these studies show, for the first time the antitumor activity of PP against breast cancer cells, in particular TNBC cells. Furthermore, it highlights the concept that optimal treatment of TNBC warrants attention to the differential sensitivity of various TNBC subtypes to therapeutic agents. These results suggest that the PP may be a potentially effective chemopreventive or therapeutic agent against breast cancer. However, additional studies are required to more fully elucidate the mechanism of antitumor effect of PP. 

Retracted: No

PubPeer comments:
 Figure 5. Some panels appear to show areas of overlap. Areas that appear similar are shown with boxes of the same color. Dotted line indicates a flipped image. ![file] ,
PKMYT1 aggravates the progression of ovarian cancer by targeting SIRT3
Authors: H-Y Zhang
Z-H Xuan
X-N Zhang
Z-X Chen
M-M Gu
H-P Wang
Journal: European review for medical and pharmacological sciences (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: PKMYT1; ovarian cancer; metastasis; prognosis; SIRT3
Affiliations: Department of Obstetrics and Gynecology, Jinan Second Maternal and Child Health Hospital, Jinan, China. .

Abstract:  Objective: This experiment aims to elucidate the role of PKMYT1 in the malignant progression of ovarian cancer (OC) and its underlying mechanism. Patients and methods: Expression pattern of PKMYT1 in 43 paired OC tissues and adjacent normal ones was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The potential relationship between PKMYT1 level and clinical data of OC patients was analyzed. PKMYT1 level in OC patients either with distant metastasis or not was examined. Through Cell Counting Kit (CCK-8) and transwell assay, influences of PKMYT1 on proliferative and metastatic abilities in 3AO and CAOV3 cells were assessed. At last, the role of PKMYT1/SIRT3 regulatory loop in the progression of OC was identified. Results: PKMYT1 was upregulated in OC tissues relative to controls. OC patients accompanied with distant metastasis had higher abundance of PKMYT1. High level of PKMYT1 predicted worse prognosis in OC patients. Knockdown of PKMYT1 attenuated proliferative, migratory, and invasive abilities in OC cells. Moreover, SIRT3 was downregulated in OC tissues, which was negatively correlated to PKMYT1. Silencing of SIRT3 could abolish the regulatory effect of PKMYT1 on proliferative and metastatic abilities in OC. Conclusions: Upregulated PKMYT1 in OC is closely linked to distant metastasis and poor prognosis. PKMYT1 accelerates the malignant progression of OC via negatively regulating SIRT3. 

Retracted: No

PubPeer comments:
 Two panels in Figure 2 appear to be the same. ![file] ,
Resveratrol Ameliorates Cardiac Dysfunction by Inhibiting Apoptosis via the PI3K/Akt/FoxO3a Pathway in a Rat Model of Diabetic Cardiomyopathy
Authors: Xiuli Zhang
Caiwen Ou
Zhiye Wu
Anqing Huang
Jianyun Yan
Jianwu Zhang
Qicai Liu
Minsheng Chen
Bei Liu
Journal: Journal of Cardiovascular Pharmacology (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: resveratrol; cardiac function; diabetic cardiomyopathy; apoptosis; neonatal rat ventricular myocytes
Affiliations: *Department of Cardiology, Guangdong Provincial Biomedical Engineering Technology Research Center for Cardiovascular Diseases, Zhujiang Hospital of Southern Medical University, Guangzhou, P. R. China; †Department of Histology and Embryology, Southern Medical University, Guangzhou, P. R. China; ‡Department of Cardiology, Shanghai General Hospital, Shanghai, P. R. China; and §Department of Cardiology, Nanfang Hospital of Southern Medical University, Guangzhou, P. R. China.

Abstract:  The aim of this study was to explore the effect and mechanism of action of resveratrol (RSV) on cardiac function in diabetic cardiomyopathy (DCM). Hyperglycemia-induced apoptosis contributes to the pathogenic changes in DCM. RSV treatment inhibited high glucose-induced apoptosis of neonatal rat ventricular myocytes. Additionally, high glucose decreased cell viability, prevented serine-threonine kinase (Akt) and FoxO3a phosphorylation, and suppressed cytoplasmic translocation of FoxO3a. However, these effects of apoptosis were reversed by 10 μM of RSV. The PI3K inhibitor LY294002 abolished the RSV protective effect in vitro. RSV (5 or 50 mg·kg·d orally for 8 weeks) prevented the deterioration of cardiac function and structural cardiomyopathy in a streptozotocin-induced rat model of diabetes and reduced apoptosis in diabetic myocardium. Furthermore, it restored streptozotocin-impaired phosphorylation of Akt and FoxO3a (p-Akt and p-FoxO3a) and suppressed nuclear translocation of FoxO3a in vivo. Together, these data indicate that RSV has therapeutic potential against DCM by inhibiting apoptosis via the PI3K/Akt/FoxO3a pathway. 

Retracted: No

PubPeer comments:
 Figure 4A appears to have two images which overlap with slightly different coloring. *** ![file] , 
 Similar issue in Figure 2A. *** ![file] ,
miR-221 facilitates the TGFbeta1-induced epithelial-mesenchymal transition in human bladder cancer cells by targeting STMN1
Authors: Jian Cao
Jun Liu
Xiaokun Zhao
Journal: BMC Urology (2015)
Discipline: CLINICAL MEDICINE
Keywords: metastasis; epithelial-to-mesenchymal transition (EMT); microRNAs (miRNAs); miR-221; bladder cancer
Affiliations: Department of Urology, 2nd xiangya Hospital, Central South University, NO.139 Middle Renmin Road, 410011, Changsha, Hunan, China. .

Abstract:  Background: Distant metastasis is the major cause of cancer-related death, and epithelial-to-mesenchymal transition (EMT) has a critical role in this process. Accumulating evidence indicates that EMT can be regulated by microRNAs (miRNAs). miR-221, as oncogenes in several human cancers, was significantly up-regulated in bladder cancers. However, the role of miR-221 in the progression of bladder cancer metastasis remains largely unknown. Methods: We used qRT-PCR and western blot to accurately measure the levels of miR-221, STMN1 and EMT markers in TGFβ1 induced EMT of bladder cancer cells. miR-221 inhibitors were re-introduced into bladder cancer cells to investigate its role on tumor metastasis which was measured by MTT, wound healing, transwell invasion and adherent assays. Luciferase reporter assay was used to reveal the target gene of miR-221. Results: miR-221 expression was greatly increased by TGFβ1 in bladder cancer cell. miR-221 inhibition reversed TGFβ1 induced EMT by sharply increasing the expression of the epithelial marker E-cadherin and decreasing the expression of the mesenchymal markers vimentin, Fibroactin and N-cadherin. Furthermore, miR-221 expression is positively correlated with malignant potential of bladder cancer cell through promoting loss of cell adhesion and prometastatic behavior. Luciferase reporter assay revealed that miR-221 negatively regulates STMN1 expression by direct targeting to the 3'UTR region of STMN1. Conclusions: Our study demonstrated that miR-221 facilitated TGFβ1-induced EMT in human bladder cancer cells by targeting STMN1 and represented a promising therapeutic target in the process of metastasis. 

Retracted: No

PubPeer comments:
 Figure 4: Hippocampus Week 3 and Week 1 appear to share an overlap at a different magnification. I ve added the magenta shapes to show where I mean. Would the authors please comment? ![file] ,
Case Reports of Pre-clinical Replication Studies in Metabolism and Diabetes
Authors: Allan Ertmann Karlsen
Gustaf Christoffersson
Mads Tang-Christensen
Philippe P Pagni
Kevin Grove
Matthias von Herrath
Jacob Sten Petersen
Journal: Cell Metabolism (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: reproducibility; robustness; case reports; Novo Nordisk; animal model variability
Affiliations: Novo Nordisk Research Center Seattle, Inc., Seattle, WA, USA. Electronic address: ., Novo Nordisk Research Center Seattle, Inc., Seattle, WA, USA., Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden., Novo Nordisk A/S, Måløv, Denmark.

Abstract:  Recent articles have highlighted the lack of reproducibility of data from scientific publications. Here we would argue that a better way to describe and also tackle this matter is to use the term "lack of robustness," since it points toward potential solutions. Presenting several case reports, we highlight examples with common underlying issues from Novo Nordisk's experience: animal model variability, reagent quality, and inter-lab variability. We discuss means to prevent these issues and argue for increased collaborative work and transparent manuscript revision procedures. Collectively, we believe these measures will help promote a more rapid and efficient self-corrective process in diabetes drug target research. 

Retracted: No

PubPeer comments:
 Some interesting discussion about the replication or not of the Asprosin results, including about the issue of reagent sharing. https: pubpeer.com publications 270F37381080C55C51E40C35B36026 ,
Pancreatic cancer cells overexpress gelsolin family-capping proteins, which contribute to their cell motility
Authors: H L Yin
C C Thompson
T Crnogorac-Jurcevic
F Campbell
S Patel
R E Jenkins
N R Lemoine
E Costello
W Prime
A Dodson
D Vimalachandran
G Saraga
F J Ashcroft
Journal: Gut (2007)
Discipline: CLINICAL MEDICINE
Keywords: proteomic methods; pancreatic ductal adenocarcinoma; CapG; gelsolin; metastatic pancreatic cancer
Affiliations: Division of Surgery and Oncology, Royal Liverpool University Hospital, 5th Floor UCD Building, Daulby Street, University of Liverpool, Liverpool L68 3 GA, UK.

Abstract:  Background: Previously, proteomic methods were applied to characterise differentially expressed proteins in microdissected pancreatic ductal adenocarcinoma cells. Aims: To report that CapG and a related protein, gelsolin, which have established roles in cell motility, are overexpressed in metastatic pancreatic cancer; and to describe their pattern of expression in pancreatic cancer tissue and their effect on cell motility in pancreatic cancer cell lines. Methods: CapG was identified by mass spectrometry and immunoblotting. CapG and gelsolin expression was assessed by immunohistochemical analysis on a pancreatic cancer tissue microarray and correlated with clinical and pathological parameters. CapG and gelsolin levels were reduced using RNA interface in Suit-2, Panc-1 and MiaPaCa-2 cells. Cell motility was assessed using modified Boyden chamber or wound-healing assays. Results: Multiple isoforms of CapG were detected in pancreatic cancer tissue and cell lines. Immunohistochemical analysis of benign (n = 44 patients) and malignant (n = 69) pancreatic ductal cells showed significantly higher CapG staining intensity in nuclear (p&lt;0.001) and cytoplasmic (p&lt;0.001) compartments of malignant cells. Similarly, gelsolin immunostaining of benign (n = 24 patients) and malignant (n = 68 patients) pancreatic ductal cells showed higher expression in both compartments (both p&lt;0.001). High nuclear CapG was associated with increased tumour size (p = 0.001). High nuclear gelsolin was associated with reduced survival (p = 0.01). Reduction of CapG or gelsolin expression in cell lines by RNAi was accompanied by significantly impaired motility. Conclusions: Up regulation of these actin-capping proteins in pancreatic cancer and their ability to modulate cell motility in vitro suggest their potentially important role in pancreatic cancer cell motility and consequently dissemination. 

Retracted: No

PubPeer comments:
 A hard to explain duplication of a single Western blot band in Figure 4b. ![file] ,
Uncovering transcriptional dark matter via gene annotation independent single-cell RNA sequencing analysis
Authors: Jonathan T Butcher
Charles G Danko
Madhav Mantri
David W McKellar
Gaetano J Scuderi
Michael F Z Wang
Iwijn De Vlaminck
Shao-Pei Chou
Journal: Nature Communications (2021)
Discipline: Multidisciplinary
Keywords: scRNA-seq; genome annotation; transcriptional activity; single-cell expression matrix; transcriptionally active regions (TARs)
Affiliations: Nancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, Ithaca, NY, 14853, USA., Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA., Nancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, Ithaca, NY, 14853, USA. .

Abstract:  Conventional scRNA-seq expression analyses rely on the availability of a high quality genome annotation. Yet, as we show here with scRNA-seq experiments and analyses spanning human, mouse, chicken, mole rat, lemur and sea urchin, genome annotations are often incomplete, in particular for organisms that are not routinely studied. To overcome this hurdle, we created a scRNA-seq analysis routine that recovers biologically relevant transcriptional activity beyond the scope of the best available genome annotation by performing scRNA-seq analysis on any region in the genome for which transcriptional products are detected. Our tool generates a single-cell expression matrix for all transcriptionally active regions (TARs), performs single-cell TAR expression analysis to identify biologically significant TARs, and then annotates TARs using gene homology analysis. This procedure uses single-cell expression analyses as a filter to direct annotation efforts to biologically significant transcripts and thereby uncovers biology to which scRNA-seq would otherwise be in the dark. 

Retracted: No

PubPeer comments:
 Without reading this paper in full detail, I recalled that [Ding et al, in Systematic comparative analysis of single cell RNA-sequencing methods] , found that: u201cInterestingly, 10x Chromium (v2) had the highest fraction of antisense reads (33% and 29%), followed by DroNc-seq (10% and 12%), and sci-RNA-seq (6% and 9%; Supplementary Fig. 3c). We did not observe this level of antisense reads in bulk cortex nuclei nor in PBMC scRNA-seq datasets (data not shown). We excluded these antisense reads from our subsequent analysis. Suggesting that either - 10X is specifically capable of detecting these reads better than all others, or - It is an artifact of 10X. Ding et al opted for this. ----- An interesting note is that using pre-mRNA gene models one get much more antisense reads. [From 10X] [Antisense fraction] may be higher if using a pre- mRNA reference or may indicate incorrect Gel Bead chemistry. ,