PReD-Bench/PRed-Bench huggingface dataset:
RNA-mediated thermoregulation of iron-acquisition genes in Shigella dysenteriae and pathogenic Escherichia coli
Authors: Franz Narberhaus
Jens Kortmann
Francesco Righetti
Andrew B Kouse
Erin R Murphy
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: iron acquisition; heme utilization; ShuA; temperature regulation; post-transcriptional regulation
Affiliations: Ohio University, Department of Biology, Molecular Cell Biology Program. Athens, Ohio, United States of America.

Abstract:  The initiation, progression and transmission of most bacterial infections is dependent upon the ability of the invading pathogen to acquire iron from each of the varied environments encountered during the course of a natural infection. In total, 95% of iron within the human body is complexed within heme, making heme a potentially rich source of host-associated nutrient iron for invading bacteria. As heme is encountered only within the host, pathogenic bacteria often regulate synthesis of heme utilization factors such that production is maximal under host-associated environmental conditions. This study examines the regulated production of ShuA, an outer-membrane receptor required for the utilization of heme as a source of nutrient iron by Shigella dysenteriae, a pathogenic bacterium that causes severe diarrheal diseases in humans. Specifically, the impact of the distinct environmental temperatures encountered during infection within a host (37°C) and transmission between hosts (25°C) on shuA expression is investigated. We show that shuA expression is subject to temperature-dependent post-transcriptional regulation resulting in increased ShuA production at 37°C. The observed thermoregulation is mediated by nucleic acid sequences within the 5' untranslated region. In addition, we have identified similar nucleotide sequences within the 5' untranslated region of the orthologous chuA transcript of enteropathogenic E. coli and have demonstrated that it also functions to confer temperature-dependent post-transcriptional regulation. In both function and predicted structure, the regulatory element within the shuA and chuA 5' untranslated regions closely resembles a FourU RNA thermometer, a zipper-like RNA structure that occludes the Shine-Dalgarno sequence at low temperatures. Increased production of ShuA and ChuA in response to the host body temperature allows for maximal production of these heme acquisition factors within the environment where S. dysenteriae and pathogenic E. coli strains would encounter heme, a host-specific iron source. 

Retracted: No

PubPeer comments:
 Lane 1 in panel A in Figure 6 looks similar to lane 1 in Panel 7C if one of the two is rotated 180 degrees. Note the presence of some small dots, highlighted with diagonal arrows. Sharp vertical background transitions are visible between lanes 1 and 2 in both panels. ![file] ,
Clinical Characteristics and Blood Test Results in COVID-19 Patients
Authors: Jun-Yan Zhao
Xu-Sheng An
Fu-Tai Shang
Xiang-Yu Li
Shu-Feng Yang
Hong-Gang Wang
Xiao-Zhong Yang
Journal: Annals of clinical and laboratory science (2020)
Discipline: CLINICAL MEDICINE
Keywords: COVID-19; blood test; coronavirus; hospital stay; pneumonia.
Affiliations: Intensive Care Unit, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, China., Department of Gastroenterology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, China., Department of Infectious Diseases and Intensive Care Unit, Huai'an Fourth People's Hospital, Huai'an, Jiangsu Province, China., Department of Gastroenterology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, China .

Abstract:  Objective: An outbreak of pneumonia named COVID-19 caused by a novel coronavirus in Wuhan is rapidly spreading worldwide. The objective of the present study was to clarify further the clinical characteristics and blood parameters in COVID-19 patients. Materials and methods: Twenty-three suspected patients and 64 patients with laboratory-confirmed SARS-Cov-2 infection were admitted to a designated hospital. Epidemiological, clinical, laboratory, and treatment data were collected and analyzed. Results: Of the 64 patients studied, 47 (73.4%) had been exposed to a confirmed source of COVID-19 transmission. On admission, the most common symptoms were fever (75%) and cough (76.6%). Twenty-eight (43.8%) COVID-19 patients showed leukopenia, 10 (15.6%) showed lymphopenia, 47 (73.4%) and 41 (64.1%) had elevated high-sensitivity C-reactive protein (hsCRP) and erythrocyte sedimentation rate (ESR), respectively, and 30 (46.9%) had increased fibrinogen concentration. After the treatment, the counts of white blood cells and platelets, and the level of prealbumin increased significantly, while aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and hsCRP decreased. COVID-19 patients with the hospital stay longer than 12 days had higher body mass index (BMI) and increased levels of AST, LDH, fibrinogen, hsCRP, and ESR. Conclusions: Results of blood tests have potential clinical value in COVID-19 patients. 

Retracted: Yes

PubPeer comments:
 **Retracted** on July 1, 2020: http: www.annclinlabsci.org content 50 4 560.extract#  *The manuscript  Clinical Characteristics and Blood Test Results in COVID-19 Patients (by Xu-Sheng An, Xiang-Yu Li, Fu-Tai Shang, Shu-Feng Yang, Jun-Yan Zhao, Xiao-Zhong Yang, and Hong-Gang Wang) published in Annals of Clinical and Laboratory Science, vol. 50 # 3, 2020; pp. 299-307 has been retracted by the request of the authors. Statement of the authors:  There are errors in the laboratory data of COVID-19 patients. Most of the laboratory data of COVID-19 patients were incorrectly entered into statistical software, which led to errors in the results and conclusions of the study . This article is no longer available.* , 
 US$7.00 to access the PDF. ,
WITHDRAWN: Novel research opportunities 2: An unfortunate small silver lining to COVID-19
Authors: Victor Grech
Sarah Cuschieri
Journal: Early Human Development (2020)
Discipline: CLINICAL MEDICINE
Keywords: Article withdrawal; Author; Editor; Publisher; Elsevier Policy
Affiliations: Mater Dei Hospital, Malta. Electronic address: ., Faculty of Medicine and Surgery, University of Malta, Malta. Electronic address: .

Abstract:  This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal. 

Retracted: No

PubPeer comments:
 Withdrawn: https: www.sciencedirect.com science article pii S0378378220307532?dgcid=rss_sd_all  This article has been withdrawn at the request of the author(s) and or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https: www.elsevier.com about our-business policies article-withdrawal. For more details see Retraction Watch coverage: https: retractionwatch.com 2021 03 31 beam-us-up-elsevier-pulls-26-covid-19-papers-by-researcher-with-a-penchant-for-star-trek ,
In vitro and in vivo antioxidant potentials of an ethanolic extract of Ganoderma lucidum in rat mammary carcinogenesis
Authors: S Mirunalini
K Deepalakshmi
V Arulmozhi
M Krishnaveni
Journal: Chinese Journal of Natural Medicines (2013)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: ABTS (2, 2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid); Antioxidant activity; DPPH (2, 2-diphenyl-2-picrylhydrazyl); Free radicals; Ganoderma lucidum.

Abstract:  Aim: Considering the importance of diet in the prevention of cellular damage caused by reactive oxygen species which has been implicated for several diseases, this present study was undertaken to evaluate the in vitro and in vivo antioxidant potential of the ethanolic extract of the fruiting bodies of Ganoderma lucidum on 7, 12-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinogenesis in Sprague Dawley rats. Methods: Ganoderma lucidum extract was tested for in vitro antioxidant and radical scavenging assays, such as (ABTS(+)) radical cation decolorization assay, DPPH radical scavenging, hydroxyl radical, and superoxide radical scavenging assays. The in vivo antioxidant potentials were analyzed by SOD, CAT, and GPx in plasma, mammary, and liver tissues. Results: In all the in vitro antioxidant and radical scavenging assays the extract exhibited good scavenging activity. In vivo enzymatic antioxidant levels, such as SOD, CAT, and GPx were decreased in DMBA-induced animals. Moreover, pretreatment with G. lucidum (500 mg · kg(-1) bw) to DMBA-induced animals significantly (P &lt; 0.05) increased the levels of SOD, CAT, and GPx in plasma, mammary, and liver tissues compared to DMBA induced animals. Conclusions: From these findings, it is suggested that G. lucidum extract could be considered as a potential source of natural antioxidants and can be used as an effective chemopreventive agent against mammary cancer. 

Retracted: No

PubPeer comments:
 This paper is one of several from this research group at the Department of Biochemistry and Biotechnology of Annamalai University that reports measurements with an unexpectedly narrow range of standard deviations (SDs). Table 1 shows the effect of a mushroom extract on control and tumor-induced rats. ![file] The SDs all fall within an unexpectedly narrow range, with a mean of 7.8% of the measurements. Here is the histogram of the SDs: ![file] Could the authors please provide the raw data? , 
 Figures 2 through 5 show different types of scavenging percentages, displaying the average of three measurements. However, no SDs or other types of error bars are shown. ![file] This and other unexpectedly narrow ranges of SDs makes one wonder if the experiments from this group really include replicate measurements. , 
 Update for comment #1: For comparison, here is a collage of 12 papers from other research groups to show the expected range of SDs. All of these use groups of 6 to 8 rats, and do similar measurements. I graphed their SDs in the same way as the graph above, but with the X axis up to 100%. Each of these graphs show a much wider and more even spread of SDs than the graph above. ![file] ,
Hepatocyte growth factor-induced expression of ornithine decarboxylase, c-met, and c-myc is differently affected by protein kinase inhibitors in human hepatoma cells HepG2
Authors: G Pogliaghi
M A Desiderio
P Dansi
Journal: Experimental Cell Research (1998)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Hepatocyte growth factor; HGF; c-met; gene expression; protein kinase
Affiliations: Institute of General Pathology and CNR Center for Research on Cell Pathology, University of Milano, via Mangiagalli, Milan, 31-20133, Italy. 

Abstract:  Binding of hepatocyte growth factor (HGF) to its receptor Met induces autophosphorylation and activation of the tyrosine kinase activity. In HGF-treated HepG2 cells, we studied: (i) the expression patterns of early (c-myc, c-jun, and c-fos) and delayed-early (ornithine decarboxylase and c-met) response genes and (ii) the possible involvement of protein kinase transducers in the control of the expression of c-met and of other genes eventually induced downstream. c-met and c-myc mRNAs peaked 1-2 h after HGF, while c-jun and c-fos mRNAs slightly increased at 1 h. Ornithine decarboxylase activity was induced earlier (4 h) than the mRNA (8-10 h). The transducers involved in HGF-triggered gene inductions were investigated using different protein kinase inhibitors: genistein for the receptor tyrosine kinase, herbimycin A for the nonreceptor tyrosine kinase (pp60(c-src)), wortmannin for phosphatidylinositol 3-kinase (PI3K) and H7 for protein kinase C (PKC). The similarity of responses to PKC inhibition led to suppose that c-myc and ornithine decarboxylase mRNAs were induced sequentially along the same transduction pathway triggered by HGF. Ornithine decarboxylase activity seemed to be largely regulated by phosphorylation(s). The mRNA expression of c-jun was likely to undergo a negative regulation through a mechanism involving PI3K, while that of c-met seemed to be almost independent from various protein kinases (PI3K, pp60(c-src), and PKC). 

Retracted: Yes

PubPeer comments:
 Figures 1 and 5. https: imgur.com Snq26ma , 
 ![file] , 
 2020 retraction. https: www.sciencedirect.com science article pii S0014482720304237?via%3Dihub This article has been retracted at the request of the Editor-in-Chief and the authors as lanes of Figure 1 are similar with lanes of Figure 5 of this article and Figure 4B of the article that the authors have published in the Journal of Cellular Physiology 174 (1998) 125u2013134 https: doi.org 10.1002 (SICI)1097-4652(199801)174:1 125::AID-JCP14 3.0.CO;2-E. ,
LINC00665/miR-9-5p/ATF1 is a novel axis involved in the progression of colorectal cancer
Authors: Weijie Pan
Yin Long
Zhi Li
Xuhong Zhao
Fenyong Sun
Wenhao Weng
Journal: Human Cell (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ATF1; CRC; LINC00665; miR-9-5p.
Affiliations: Department of Clinical Laboratory, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, People's Republic of China., Department of Clinical Laboratory, Yangpu Hospital, Tongji University School of Medicine, Shanghai, 200090, People's Republic of China. ., Department of Clinical Laboratory, Shanghai 10th People's Hospital, Tongji University School of Medicine, No. 301 Middle Yanchang Road, Shanghai, 200072, People's Republic of China. .

Abstract:  Long noncoding RNAs (lncRNAs) are abnormally expressed in many malignant tumors and involved in regulating the malignant phenotypes of cancer cells. However, the role of LINC00665 in colorectal cancer (CRC) and its regulatory mechanism remain unclear. In this study, real-time polymerase chain reaction (RT-PCR) was used to detect the expressions of LINC00665, miR-9-5p and activating transcription factor 1 (ATF1) mRNA in CRC tissues. The expression of ATF1 in CRC tissues was also detected by immunohistochemistry and Western blot. CCK-8 and colony formation assays were employed to detect cell proliferation. Cell cycle and apoptosis were detected by flow cytometry analysis. Scratch healing assay and Transwell test were exploited to detect cell migration and invasion. The targeting relationships between LINC00665 and miR-9-5p, and miR-9-5p and ATF1 were validated by dual luciferase reporter assay. We found that LINC00665 was significantly overexpressed in CRC tissues, and it was also negatively correlated with the expression of miR-9-5p and positively associated with the expression of ATF1. Besides, LINC00665 promoted the proliferation, migration and invasion of CRC cells, and inhibited cell apoptosis by sponging miR-9-5p. ATF1 was proved to be the downstream target of miR-9-5p and was indirectly regulated by LINC00665. Collectively, it is concluded that LINC00665 contributes to the progression of CRC by regulating miR-9-5p/ATF1 axis. 

Retracted: No

PubPeer comments:
 Overlap was detected in Fig.4b and 4c ![file] ,
HBx induces HepG-2 cells autophagy through PI3K/Akt–mTOR pathway
Authors: Qing-Song Guo
Zhi-Wei Wang
Peng Wang
Hai-Xin Qian
Journal: Molecular and Cellular Biochemistry (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Chronic hepatitis B virus infection; hepatocellular carcinoma; HBx protein; cell cycle progression; tumor suppressor genes
Affiliations: Department of Hepatobiliary Surgery, First Affiliated Hospital of Soochow University, Suzhou 215004, People's Republic of China. 

Abstract:  Chronic hepatitis B virus infection is the dominant global cause of hepatocellular carcinoma (HCC), especially hepatitis B virus-X (HBx) plays a major role in this process. HBx protein promotes cell cycle progression, inactivates negative growth regulators, and binds to and inhibits the expression of p53 tumor suppressor gene and other tumor suppressor genes and senescence-related factors. However, the relationship between HBx and autophagy during the HCC development is poorly known. Previous studies found that autophagy functions as a survival mechanism in liver cancer cells. We suggest that autophagy plays a possible role in the pathogenesis of HBx-induced HCC. The present study showed that HBx transfection brought about an increase in the formation of autophagosomes and autolysosomes. Microtubule-associated protein light chain 3, Beclin 1, and lysosome-associated membrane protein 2a were up-regulated after HBx transfection. HBx-induced increase in the autophagic level was increased by mTOR inhibitor rapamycin and was blocked by treatment with the PI3K-Akt inhibitor LY294002. The same results can also be found in HepG2.2.15 cells. These results suggest that HBx activates the autophagic lysosome pathway in HepG-2 cells through the PI3K-Akt-mTOR pathway. 

Retracted: No

PubPeer comments:
 Figures 1A and 3A. * Red boxes: Two panels, labeled differently, appear to look the same. ![file] Figures 1B, 2, 3B, 5. * Blue, green, purple boxes: Western blot panels look more similar than expected. ![file] Reported to the journal in October 2015, with a friendly reminder in 2017, but no response as of today. ,
Neratinib degrades MST4 via autophagy that reduces membrane stiffness and is essential for the inactivation of PI3K, ERK1/2, and YAP/TAZ signaling
Authors: Andrew Poklepovic
Laurence Booth
John F Hancock
Paul Dent
Jennifer Martinez
Daniel Von Hoff
Journal: Journal of cellular physiology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ERK; HDAC inhibitor; Hippo; Merlin; PI3K
Affiliations: Departments of Biochemistry and Molecular Biology, Virginia Commonwealth University, Richmond, Virginia., Medicine, Virginia Commonwealth University, Richmond, Virginia., Inflammation & Autoimmunity Group, National Institute of Environmental Health Sciences, Triangle Park, North Carolina., Translational Genomics Research Institute (TGEN), Phoenix, Arizona., Department of Integrative Biology and Pharmacology, University of Texas Health Science Center, Houston, Texas.

Abstract:  The irreversible ERBB1/2/4 inhibitor neratinib causes plasma membrane-associated K-RAS to mislocalize into intracellular vesicles liminal to the plasma membrane; this effect is enhanced by HDAC inhibitors and is now a Phase I trial (NCT03919292). The combination of neratinib and HDAC inhibitors killed pancreatic cancer and lymphoma T cells. Neratinib plus HDAC inhibitor exposure was as efficacious as (paclitaxel+gemcitabine) at killing pancreatic cancer cells. Neratinib reduced the phosphorylation of PAK1, Merlin, LATS1/2, AKT, mTOR, p70 S6K, and ERK1/2 which required expression of Rubicon, Beclin1, and Merlin. Neratinib altered pancreatic tumor cell morphology which was associated with MST4 degradation reduced Ezrin phosphorylation and enhanced phosphorylation of MAP4K4 and LATS1/2. Knockdown of the MAP4K4 activator and sensor of membrane rigidity RAP2A reduced basal LATS1/2 and YAP phosphorylation but did not prevent neratinib from stimulating LATS1/2 or YAP phosphorylation. Beclin1 knockdown prevented MST4 degradation, Ezrin dephosphorylation and neratinib-induced alterations in tumor cell morphology. Our findings demonstrate that neratinib enhances LATS1/2 phosphorylation independently of RAP2A/MAP4K4 and that MST4 degradation and Ezrin dephosphorylation may represent a universal trigger for the biological actions of neratinib. 

Retracted: No

PubPeer comments:
 The effect of neratinib shown in Figure 5 is not very convincing. The examples you present by increasing the brightness to illustrate the difference is misleading. If you play with the brightness with other cells treated with neratinib shown in the figure, you will see nice filamentous projections. Is it simply a play with the brightness? In Figure 7, when playing with the brightness, you see the same colocalization for control vs neratinib treated cells. In Figure 2 you only show one single cell. Why not showing several? ![file] ,
Identification of the targets of hematoporphyrin derivative in lung adenocarcinoma using integrated network analysis
Authors: Yan Yu
Hongtao Yin
Journal: Biological research (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Hematoporphyrin derivative; Integrated network; Lung adenocarcinoma; Protein–protein interaction network; X-ray.

Abstract:  Background: Hematoporphyrin derivative (HPD) has a sensibilization effect in lung adenocarcinoma. This study was conducted to identify the target genes of HPD in lung adenocarcinoma. Methods: RNA sequencing was performed using the lung adenocarcinoma cell line A549 after no treatment or treatment with X-ray or X-ray + HPD. The differentially expressed genes (DEGs) were screened using Mfuzz package by noise-robust soft clustering analysis. Enrichment analysis was carried out using "BioCloud" online tool. Protein-protein interaction (PPI) network and module analyses were performed using Cytoscape software. Using WebGestalt tool and integrated transcription factor platform (ITFP), microRNA target and transcription factor (TF) target pairs were separately predicted. An integrated regulatory network was visualized with Cytoscape software. Results: A total of 815 DEGs in the gene set G1 (continuously dysregulated genes along with changes in processing conditions [untreated-treated with X-ray-X-ray + treated with HPD]) and 464 DEGs in the gene set G2 (significantly dysregulated between X-ray + HPD-treated group and untreated/X-ray-treated group) were screened. The significant module identified from the PPI network for gene set G1 showed that ribosomal protein L3 (RPL3) gene could interact with heat shock protein 90 kDa alpha, class A member 1 (HSP90AA1). TFs AAA domain containing 2 (ATAD2) and protein inhibitor of activated STAT 1 (PIAS1) were separately predicted for the genes in gene set G1 and G2, respectively. In the integrated network for gene set G2, ubiquitin-specific peptidase 25 (USP25) was targeted by miR-200b, miR-200c, and miR-429. Conclusion: RPL3, HSP90AA1, ATAD2, and PIAS1 as well as USP25, which is targeted by miR-200b, miR-200c, and miR-429, may be the potential targets of HPD in lung adenocarcinoma. 

Retracted: No

PubPeer comments:
 In Figure 1b, a flow cytometry dot plot has been duplicated and presented as something else. A blind peer review, literally? ![file] , 
 We are correcting. Thanks! ,
p14 ARF Activates a Tip60-Dependent and p53-Independent ATM/ATR/CHK Pathway in Response to Genotoxic Stress
Authors: Elisabeth Brambilla
Edwige Col
Saadi Khochbin
Camille Leduc
Caroline Salon
Paule Claverie
Sylvie Gazzeri
Béatrice Eymin
Journal: Molecular and Cellular Biology (2006)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p14ARF; tumor suppressor; p53; Mdm2; G2 cell cycle arrest
Affiliations: Groupe de Recherche sur le Cancer du Poumon, INSERM U578, Institut Albert Bonniot, 38706 La Tronche Cedex, France., INSERM U578, Institut Albert Bonniot, Université Joseph Fourier, Faculté de Medecine, Groupe de Recherche sur le Cancer du Poumon, 38706 La Tronche Cedex, France, INSERM U309, Institut Albert Bonniot, Université Joseph Fourier, Laboratoire de Biologie Moléculaire et Cellulaire de la Différenciation, 38706 La Tronche Cedex, France

Abstract:  p14ARF is a tumor suppressor that controls a well-described p53/Mdm2-dependent checkpoint in response to oncogenic signals. Here, new insights into the tumor-suppressive function of p14ARF are provided. We previously showed that p14ARF can induce a p53-independent G2 cell cycle arrest. In this study, we demonstrate that the activation of ATM/ATR/CHK signaling pathways contributes to this G2 checkpoint and highlight the interrelated roles of p14ARF and the Tip60 protein in the initiation of this DNA damage-signaling cascade. We show that Tip60 is a new direct p14ARF binding partner and that its expression is upregulated and required for ATM/CHK2 activation in response to p14ARF. Strikingly, both p14ARF and Tip60 products accumulate following a cell treatment with alkylating agents and are absolutely required for ATM/CHK2 activation in this setting. Moreover, and consistent with p14ARF being a determinant of CHK2 phosphorylation in lung carcinogenesis, a strong correlation between p14ARF and phospho-CHK2 (Thr68) protein expression is observed in human lung tumors (P &lt; 0.00006). Overall, these data point to a novel regulatory pathway that mediates the p53-independent negative-cell-growth control of p14ARF. Inactivation of this pathway is likely to contribute to lung carcinogenesis. 

Retracted: No

PubPeer comments:
 Figures 6A and 7A. Much more similar than you would expect. ![file] , 
 ![file] , 
 #1 Figure 6A. ATR panel. Much more similar than you would expect. ![file] , 
 Figure 7C. Much more similar than you would expect. ![file] , 
 #1 6A. ATR panel. Detail. https: imgur.com jJ8OBXJ , 
 Thank you for your comment. We are considering it seriously. The matter is now under investigation. Information on the outcome and appropriate responses will be posted in the close future. , 
 Figure 4A. Much more similar than expected. ![file] , 
 #6 Is there an update on this? Is the original data available? The concerns seem very clear and consequential. *** 6A. ATR panel. Detail. False color. ![file] ,
Physcion induces apoptosis in hepatocellular carcinoma by modulating miR-370
Authors: Yan Li
Dongmeng Tong
Chen Wang
Li Sun
Xiaoping Pan
Lida Zhu
Chunjuan Zhao
Haixia Wang
Di Wu
Journal: American journal of cancer research (2016)
Discipline: CLINICAL MEDICINE
Keywords: DNMT1; Physcion; apoptosis; miR-370.
Affiliations: The People's Hospital of Wuhai Inner Mongolia, PR China., The Mongolian medical & TCM Hospital of Wuhai Inner Mongolia, PR China.

Abstract:  Hepatocellular carcinoma (HCC) is one of the most common and aggressive malignancies. The current study is designed to explore the role of physcion, a major active ingredient in several traditional herbal medicinal plants, for the treatment of HCC. HCC cell lines, SMMC7721 and HepG2, were treated with physcion and its apoptosis-inducing effect was examined. Both in vitro and in vivo results from the present study demonstrated that physcion treatment resulted in apoptotic cell death in HCC cells via upregulation of miR-370. Furthermore, our findings showed that the physcion modulated the level of miR-370 through AMPK/Sp1/DNMT1 signaling. Taken together, these results showed that physcion exerts anti-tumor effect against HCC, which may be a potential agent for the adjunct chemotherapy. 

Retracted: No

PubPeer comments:
 Fig 5G,  AMPK Sp1 DNMT1 signaling is involved in physcion-induced apoptosis of HCC cells . ![file] These images, relabelled and sometimes slightly modified, subsequently reappeared frequently within this oeuvre of papers. For instance, 5C of [Gao et al (2017)] : ![file] ,
LncRNA TUG1 promotes the progression of colorectal cancer via the miR-138-5p/ZEB2 axis
Authors: Sen Hong
Qiyu Zhang
Zhenkun Yan
Miaomiao Bi
Yumei Song
Journal: Bioscience Reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CRC; TUG1; ZEB2; biological function; miR-138-5p.
Affiliations: Department of Endoscopy Center, China-Japan Union Hospital of Jilin University, Changchun 130022, Jilin Province, P.R. China, Department of Ophthalmology, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China, Department of Radiology, Jilin Oil Field Hospital, SongYuan, Jilin138000, P.R. China, Department of Thoracic Oncology, Tumor Hospital of Jilin Province, Jilin 130000, P.R. China, Department of Colorectal and Anal Surgery, The First Hospital of Jilin University, Changchun130021, Jilin Province, P.R. China

Abstract:  To explore the role of long-chain non-coding RNA (lncRNA) taurine up-regulated gene 1 (TUG1) in the development of colorectal cancer (CRC) via the miR-138-5p/zinc finger E-box-binding homeobox 2 (ZEB2) axis. Eighty-four CRC tissue specimens and 84 corresponding paracancerous tissue specimens were sampled from 84 patients with CRC admitted to the First Hospital of Jilin University from January 2018 to September 2019. The TUG1 expression in the specimens was determined, and its value in diagnosis and prognosis of CRC was analyzed. Additionally, constructed stable and transient overexpresison vectors and inhibition vectors were transfected into CRC cells. The MTT, transwell, and flow cytometry were adopted for analysis on the proliferation, invasion, and apoptosis of transfected cells, respectively, and a dual luciferase reporter (DLR) assay was carried out for correlation determination between TUG1 and miR-138-5p and between miR-138-5p and ZEB2. TUG1 was up-regulated in CRC, and serum TUG1 could be adopted as a diagnostic marker of CRC, with area-under-the-curve (AUC) larger than 0.8. In addition, siRNA-TUG1, shRNA-TUG1, miR-138-5p-mimics, and miR-138-5p-inhibitor were transfected into cells, and it turned out that overexpressing miR-138-5p and inhibiting ZEB2 exerted the same effects. The DLR assay revealed that TUG1 was able to targetedly regulate miR-138-5p, and miR-138-5p could targetedly regulate ZEB2, and in vitro experiments revealed that TUG1 could affect the epithelial-to-mesenchymal transition (EMT) of CRC via the miR-138-5p/ZEB2 axis. TUG1 could promote the development of CRC via the miR-138-5p/ZEB2 axis. 

Retracted: No

PubPeer comments:
 Figure 1A and 1D look the same. Could the author check if a wrong chart is placed? ![file] , 
 April 6, 2021 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. ,
Catalpol inhibits TGF‐β1‐induced epithelial‐mesenchymal transition in human non–small‐cell lung cancer cells through the inactivation of Smad2/3 and NF‐κB signaling pathways
Authors: Bo Sheng
Yi Lu
Yi Ding
Zuopei Wang
Xiaoke Cheng
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: catalpol; epithelial-mesenchymal transition; metastasis; non-small-cell lung cancer; transforming growth factor β1.
Affiliations: Department of Thoracic Surgery, Shanghai Pudong New Area People's Hospital, Shanghai, China., Department of Scientific Research, Shanghai Pudong New Area People's Hospital, Shanghai, China.

Abstract:  Catalpol, one of the main active ingredients isolated from Rehmannia glutinosa, was reported to possess anticancer activity. However, the role of catalpol in transforming growth factor β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) in human non-small-cell lung cancer (NSCLC) cells has not been elucidated. The objective of this study was to investigate the effect of catalpol on EMT in human NSCLC cells. Our results showed that catalpol significantly inhibited the TGF-β1-induced cell migration and invasion of A549 cells, as well as repressed matrix metalloproteinase (MMP)2 and MMP9 expression induced by TGF-β1 in A549 cells. In addition, catalpol markedly repressed the EMT process in A549 cells in response to TGF-β1. Furthermore, catalpol prevented the activation of Smad2/3 and nuclear factor κB (NF-κB) signaling pathways induced by TGF-β1 in A549 cells. In conclusion, these findings indicated that catalpol inhibits TGF-β1-induced EMT in human NSCLC cells through the inactivation of Smad2/3 and NF-κB signaling pathways. Thus, catalpol may be a promising agent for the treatment of NSCLC. 

Retracted: No

PubPeer comments:
 Fig 2A.  Cell migration was evaluated by the transwell migration assay . Lots of repeated visual motifs. I have left two panels as an exercise for the reader. ![file] ,
Evidence of a Ceiling Effect for Training Volume in Muscle Hypertrophy and Strength in Trained Men - Less is More?
Authors: Paulo Gentil
Jurgen Giessing
James P Fisher
Matheus Barbalho
Victor Silveira Coswig
James Steele
Journal: International journal of sports physiology and performance (2020)
Discipline: CLINICAL MEDICINE
Keywords: bodybuilding; dose-response.; muscle size; muscle strength; overtraining.
Affiliations: 1 Centro de Ciências Biológicas e da Saúde, Universidade da Amazônia, Belém, Pará, Brasil., 2 Faculdade de Educação Física e Dança, Universidade Federal de Goiás, Goiânia, Goiás, Brasil., 3 Faculdade de Educação Física, Universidade Federal do Pará, Castanhal, Pará, Brasil., 4 School of Sport, Health and Social Sciences, Southampton Solent University, Southampton, UK., 5 ukactive Research Institute, London, UK., 6 Institute of Sport Science, University of Koblenz-Landau, Landau, Germany.

Abstract:  Purpose: To compare the effects of different resistance training volumes on muscle performance and hypertrophy in trained men. Methods: 37 volunteers performed resistance training for 24 weeks, divided into groups that performed five (G5), 10 (G10), 15 (G15) and 20 (G20) sets per muscle group per week. Ten repetition maximum (10RM) tests were performed for the bench press, lat pull down, 45º leg press, and stiff legged deadlift. Muscle thickness (MT) was measured using ultrasound at biceps brachii, triceps brachii, pectoralis major, quadriceps femoris and gluteus maximus. All measurements were performed at the beginning (pre) and after 12 (mid) and 24 weeks (post). Results: All groups showed significant increases in all 10RM tests and MT measures after 12 and 24 weeks when compared to pre (p &lt;0.05). There were no significant differences in any 10RM test or changes between G5 and G10 after 12 and 24 weeks. G5 and G10 showed significantly greater increases for 10RM than G15 and G20 for most exercises at 12 and 24 weeks. There were no group by time interaction for any MT measure. Conclusions: The results bring evidence of an inverted "U shaped" curve for the dose response curve for muscle strength. Whilst the same trend was noted for muscle hypertrophy, the results did not reach significance. Five to 10 sets per week might be sufficient for bringing about optimal gains in muscle size and strength in trained men over a 24-week period. 

Retracted: Yes

PubPeer comments:
 Note: this paper has now been retracted https: journals.humankinetics.com view journals ijspp 15 2 article-p268.xml?fbclid=IwAR3Cfdg520wFwwErrYSWI5mmgk_hIVhnINu-PRVDmwMfdsPPj7snfm4loAw , 
 The original retraction request stated  ...an a posteriori analysis of the data and identified inconsistencies that changed their evaluation of the results. However, for transparency I would like to state that the reason for this retraction was confirmed to me by the senior author of this paper as being the result of a research assistant who was responsible for the transfer of paper records to the spreadsheet having u201cmade much of the datau201d because he was u201ctoo busy to do the job.u201d ,
Inactivation of von Hippel-Lindau increases ovarian cancer cell aggressiveness through the HIF1α/miR-210/VMP1 signaling pathway
Authors: Xu Li
Huilian Hou
Zhen Li
Ting Liu
Wei Chen
Le Zhao
Lu Ding
Journal: International Journal of Molecular Medicine (2014)
Discipline: CLINICAL MEDICINE
Keywords: VHL; tumor suppressor gene; metastasis; cell motility; matrix metalloproteinase
Affiliations: Center for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi 710061, P.R. China., Center for Laboratory Medicine, The First Affiliated Hospital of Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi 710061, P.R. China., Department of Pathology, The First Affiliated Hospital of Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi 710061, P.R. China.

Abstract:  The inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene not only results in tumor initiation, but also mediates tumor metastasis. However, the mechanisms by which VHL inactivation leads to metastasis have not yet been well defined. In this study, the silencing of VHL in 3AO and SKOV3 ovarian cancer cells was found to promote cell motility and to increase the expression of matrix metalloproteinase (MMP)2, MMP9, hypoxia-inducible factor 1-α (HIF-1α) and microRNA (miR)-210. The suppression of HIF-1α with its inhibitor 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1) in VHL-silenced 3AO cells antagonized the pro-migratory activity induced by the VHL deficiency and reversed the upregulation of MMP2, MMP9, HIF-1α and miR-210; however, it had no obvious effect on the VHL protein level. The introduction of miR-210 inhibitor into VHL-silenced 3AO cells resulted in similar changes as those induced by YC-1. Furthermore, vacuole membrane protein 1 (VMP1) was found to be diminished by VHL silencing in a HIF-1α/miR-210-dependent manner. Taken together, our data demonstrate that the loss of VHL stimulates ovarian cancer cell migration by stabilizing HIF-1α, upregulating miR-210 and decreasing VMP1 expression. These results indicate that the aberrant signaling of the VHL/HIF-1α/miR-210/VMP1 pathway may be involved in ovarian cancer aggressiveness. 

Retracted: No

PubPeer comments:
 Figures 1C and 3A appear to have duplicated images, with the color adjusted. ![file] ![file] The treatments are different in all cases, so they should not be the same. ,
Protection of extraribosomal RPL13a by GAPDH and dysregulation by S-nitrosylation
Authors: Paul L Fox
Stanley L Hazen
Jie Jia
Abul Arif
Belinda Willard
Jonathan D Smith
Dennis J Stuehr
Journal: Molecular cell (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Ribosomal proteins; Moonlighting activities; Interferon-gamma; GAIT complex; GAPDH
Affiliations: Department of Cell Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA.

Abstract:  Multiple eukaryotic ribosomal proteins (RPs) are co-opted for extraribosomal "moonlighting" activities, but paradoxically, RPs exhibit rapid turnover when not ribosome-bound. In one illustrative case of a functional extraribosomal RP, interferon (IFN)-γ induces ribosome release of L13a and assembly into the IFN-gamma-activated inhibitor of translation (GAIT) complex for translational control of a subset of inflammation-related proteins. Here we show GAPDH functions as a chaperone, shielding newly released L13a from proteasomal degradation. However, GAPDH protective activity is lost following cell treatment with oxidatively modified low density lipoprotein and IFN-γ. These agonists stimulate S-nitrosylation at Cys(247) of GAPDH, which fails to interact with L13a, causing proteasomal degradation of essentially the entire cell complement of L13a and defective translational control. Evolution of extraribosomal RP activities might require coevolution of protective chaperones, and pathological disruption of either protein, or their interaction, presents an alternative mechanism of diseases due to RP defects, and targets for therapeutic intervention. 

Retracted: No

PubPeer comments:
 Fig3C ![file] Can authors check whether any duplication occur in L6 and L28? ,
Epidemiology and genetic diversity of bovine leukemia virus
Authors: Yoko Aida
Shin-Nosuke Takeshima
Meripet Polat
Journal: Virology Journal (2017)
Discipline: MICROBIOLOGY
Keywords: BLV diagnostic approches; BLV epidemiology; BLV genotyping methods; Bovine leukemia virus (BLV).
Affiliations: Viral Infectious Diseases Unit, RIKEN, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan., Nano Medical Engineering Laboratory, RIKEN, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan., Bovine Leukemia Virus Vaccine Laboratory RIKEN, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan., Viral Infectious Diseases Unit, RIKEN, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan. ., Nano Medical Engineering Laboratory, RIKEN, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan. ., Bovine Leukemia Virus Vaccine Laboratory RIKEN, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan. .

Abstract:  Bovine leukemia virus (BLV), an oncogenic member of the Deltaretrovirus genus, is closely related to human T-cell leukemia virus (HTLV-I and II). BLV infects cattle worldwide and causes important economic losses. In this review, we provide a summary of available information about commonly used diagnostic approaches for the detection of BLV infection, including both serological and viral genome-based methods. We also outline genotyping methods used for the phylogenetic analysis of BLV, including PCR restriction length polymorphism and modern DNA sequencing-based methods. In addition, detailed epidemiological information on the prevalence of BLV in cattle worldwide is presented. Finally, we summarize the various BLV genotypes identified by the phylogenetic analyses of the whole genome and env gp51 sequences of BLV strains in different countries and discuss the distribution of BLV genotypes worldwide. 

Retracted: No

PubPeer comments:
 I noticed a section of this 2017 paper that was copied from a 2015 paper with the same corresponding author. They have the exact same wording with same authors cited. ![file] ![file] ![file] ![file] ,
Intraarterial transplantation of human umbilical cord blood mononuclear cells is more efficacious and safer compared with umbilical cord mesenchymal stromal cells in a rodent stroke model
Authors: Kameshwar Prasad
Gary K Steinberg
Richard Schäfer
Neha Karlupia
Nathan C Manley
Journal: Stem Cell Research & Therapy (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Stroke; tissue plasminogen activator; human umbilical cord; cord blood mononuclear cells; cord blood mesenchymal stromal cells

Abstract:  Introduction: Stroke is the second leading cause of death worldwide, claims six lives every 60 seconds, and is a leading cause of adult disability across the globe. Tissue plasminogen activator, the only United States Food and Drug Administration (FDA)-approved drug currently available, has a narrow therapeutic time window of less than 5 hours. In the past decade, cells derived from the human umbilical cord (HUC) have emerged as a potential therapeutic alternative for stroke; however, the most effective HUC-derived cell population remains unknown. Methods: We compared three cell populations derived from the human umbilical cord: cord blood mononuclear cells (cbMNCs); cord blood mesenchymal stromal cells (cbMSCs), a subpopulation of cbMNCs; and cord matrix MSCs (cmMSCs). We characterized these cells in vitro with flow cytometry and assessed the cells' in vivo efficacy in a 2-hour transient middle cerebral artery occlusion (MCAo) rat model of stroke. cbMNCs, cbMSCs, and cmMSCs were each transplanted intraarterially at 24 hours after stroke. Results: A reduction in neurologic deficit and infarct area was observed in all three cell groups; however, this reduction was significantly enhanced in the cbMNC group compared with the cmMSC group. At 2 weeks after stroke, human nuclei-positive cells were present in the ischemic hemispheres of immunocompetent stroke rats in all three cell groups. Significantly decreased expression of rat brain-derived neurotrophic factor mRNA was observed in the ischemic hemispheres of all three cell-treated and phosphate-buffered saline (PBS) group animals compared with sham animals, although the decrease was least in cbMNC-treated animals. Significantly decreased expression of rat interleukin (IL)-2 mRNA and IL-6 mRNA was seen only in the cbMSC group. Notably, more severe complications (death, eye inflammation) were observed in the cmMSC group compared with the cbMNC and cbMSC groups. Conclusions: All three tested cell types promoted recovery after stroke, but cbMNCs showed enhanced recovery and fewer complications compared with cmMSCs. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Long noncoding RNA SNHG14 enhances migration and invasion of ovarian cancer by upregulating DGCR8
Authors: C-L Wang
J-L Zhao
Y-L Liu
G-Y Zhang
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Ovarian cancer; long noncoding RNAs; lncRNA SNHG14; metastasis; qRT-PCR
Affiliations: Department of Obstetrics and Gynaecology, Zhoukou Central Hospital, Zhoukou, China. .

Abstract:  Objective: Ovarian cancer is the most common fatal gynecologic malignancy in females all over the world. Recently, long noncoding RNAs (lncRNAs) have been reported to exert pivotal functions in tumorigenesis. In this research, lncRNA SNHG14 was studied to identify its role in the metastasis of ovarian cancer. Patients and methods: SNHG14 expression was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in ovarian cancer specimens. Functional assays including wound healing assay, transwell assay, and Matrigel assay were performed to detect the effect of SNHG14 on the migration and invasion of ovarian cancer cells. In addition, the underlying mechanism was further explored through qRT-PCR and Western blot assay. Results: SNHG14 level was dramatically higher in ovarian cancer specimens. Moreover, cell migration and invasion were significantly attenuated via the inhibition of SNHG14, while enhanced via the SNHG14 overexpression. Besides, the expression of DGCR8 mRNA and protein was markedly downregulated after the knockdown of SNHG14, while upregulated after SNHG14 overexpression. Furthermore, the expression level of DGCR8 was increased in cancer tissues and positively related to the expression of SNHG14 in ovarian cancer tissues. Conclusions: In summary, SNHG14 could enhance cell migration and invasion via upregulating DGCR8 in ovarian cancer. 

Retracted: No

PubPeer comments:
 Hello, I m enjoying reading this paper, great use of microscopy and a powerful new tool. Very minor error: Fig4C: Operetta measurements of activated hypnozoites with respect to EEF fluorescent surfaces (left panel) and mCherry intensity (right panel) at different days post sporozoite (spz) inoculation (green lines). For reference, the measurements of five individual primary liver stage schizonts as already are also depicted (red lines). However the image has orange and blue lines in my PDF copy, I believe the red lines are the orange ones and the green lines are the blue ones. Best wishes, Tim , 
 #1 Hi Tim, Thanks for your message and for pointing this out to us. You are absolutely right! ,
Regulation of Lung Cancer Metastasis by Klf4-Numb–like Signaling
Authors: Alice Faversani
Joseph L Kissil
Silvano Bosari
Mario Nosotti
Nina M Martin
David S Garlick
Stefano Ferrero
Valentina Vaira
Dario C Altieri
Journal: Cancer Research (2013)
Discipline: CLINICAL MEDICINE
Keywords: Metastatic traits; cancer-initiating properties; polarity protein; Numbl; tumor suppressor
Affiliations: Prostate Cancer Discovery and Development Program, The Wistar Institute, Philadelphia, PA 19104, USA.

Abstract:  Metastatic traits seem to be acquired by transformed cells with progenitor-like cancer-initiating properties, but there remains little mechanistic insight into this linkage. In this report, we show that the polarity protein Numbl, which is expressed normally in neuronal progenitors, becomes overexpressed and mislocalized in cancer cells from a variety of human tumors. Numbl overexpression relies on loss of the tumor suppressor miRNA-296-5p (miR-296), which actively represses translation of Numbl in normal cells. In turn, deregulated expression of Numbl mediates random tumor cell migration and invasion, blocking anoikis and promoting metastatic dissemination. In clinical specimens of non-small cell lung cancer, we found that Numbl overexpression correlated with a reduction in overall patient survival. Mechanistically, Numbl-mediated tumorigenesis involved suppression of a "stemness" transcriptional program driven by the stem cell programming transcription factor Klf4, thereby preserving a pool of progenitor-like cells in lung cancer. Our results reveal that Numbl-Klf4 signaling is critical to maintain multiple nodes of metastatic progression, including persistence of cancer-initiating cells, rationalizing its therapeutic exploitation to improve the treatment of advanced lung cancer. 

Retracted: No

PubPeer comments:
 Figure 2C and 2E appear to have some repeated images, after rotation. *** Enhanced contrast ![file] *** Full figure and caption ![file] ,