PReD-Bench/PRed-Bench huggingface dataset:
PML regulates p53 stability by sequestering Mdm2 to the nucleolus
Authors: Pier Paolo Scaglioni
Henning F Horn
Karen H Vousden
Pier Paolo Pandolfi
Rosa Bernardi
Stephan Bergmann
Journal: Nature Cell Biology (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PML; p53; Mdm2; nucleolus; DNA damage
Affiliations: Cancer Biology and Genetics Program, Department of Pathology and Medicine, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.

Abstract:  The promyelocytic leukaemia (PML) tumour-suppressor protein potentiates p53 function by regulating post-translational modifications, such as CBP-dependent acetylation and Chk2-dependent phosphorylation, in the PML-Nuclear Body (NB). PML was recently shown to interact with the p53 ubiquitin-ligase Mdm2 (refs 4-6); however, the mechanism by which PML regulates Mdm2 remains unclear. Here, we show that PML enhances p53 stability by sequestering Mdm2 to the nucleolus. We found that after DNA damage, PML and Mdm2 accumulate in the nucleolus in an Arf-independent manner. In addition, we found that the nucleolar localization of PML is dependent on ATR activation and phosphorylation of PML by ATR. Notably, in Pml(-/-) cells, sequestration of Mdm2 to the nucleolus was impaired, as well as p53 stabilization and the induction of apoptosis. Furthermore, we demonstrate that PML physically associates with the nucleolar protein L11, and that L11 knockdown impairs the ability of PML to localize to nucleoli after DNA damage. These findings demonstrate an unexpected role of PML in the nucleolar network for tumour suppression. 

Retracted: No

PubPeer comments:
 The abstract appears to be a product of [SCIgen] . * The artificial intelligence method to e-business is defined not only by the study of fiber-optic cables, but also by the unproven need for vacuum tubes. Given the current status of virtual archetypes, theorists clearly desire the exploration of semaphores, which embodies the compelling principles of cryptoanalysis. We present an algorithm for probabilistic theory (Buck), which we use to disprove that write-back caches can be made decentralized, lossless, and reliable. Found by the [Problematic Paper Screener] , a tool by by Guillaume Cabanac and Cyril Labbu00e9. ,
Isolation and comparative analysis of potential stem/progenitor cells from different regions of human umbilical cord
Authors: Bryan Thibodeau
Naimisha Beeravolu
G Rasul Chaudhry
Mick Perez-Cruet
Christina McKee
George Wilson
Irfan Khan
Sumi Dinda
Ray Bahado-Singh
Journal: Stem Cell Research (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Differentiation; Peri-natal stem/progenitor cells; Placenta; Proliferation; Umbilical cord.
Affiliations: Department of Biological Sciences, Oakland University, Rochester, MI 48309, USA; OU-WB Institute for Stem Cell and Regenerative Medicine, Oakland University, Rochester, MI 48309, USA., Department of Biological Sciences, Oakland University, Rochester, MI 48309, USA; OU-WB Institute for Stem Cell and Regenerative Medicine, Oakland University, Rochester, MI 48309, USA; Dr. Panjwani Center for Molecular Medicine and Drug Research, University of Karachi, Pakistan., School of Health Sciences, Oakland University, Rochester, MI 48309, USA., Beaumont Health System, Royal Oak, MI 48073, USA., OU-WB Institute for Stem Cell and Regenerative Medicine, Oakland University, Rochester, MI 48309, USA; Beaumont Health System, Royal Oak, MI 48073, USA., Department of Biological Sciences, Oakland University, Rochester, MI 48309, USA; OU-WB Institute for Stem Cell and Regenerative Medicine, Oakland University, Rochester, MI 48309, USA. Electronic address: .

Abstract:  Human umbilical cord (hUC) blood and tissue are non-invasive sources of potential stem/progenitor cells with similar cell surface properties as bone marrow stromal cells (BMSCs). While they are limited in cord blood, they may be more abundant in hUC. However, the hUC is an anatomically complex organ and the potential of cells in various sites of the hUC has not been fully explored. We dissected the hUC into its discrete sites and isolated hUC cells from the cord placenta junction (CPJ), cord tissue (CT), and Wharton's jelly (WJ). Isolated cells displayed fibroblastoid morphology, and expressed CD29, CD44, CD73, CD90, and CD105, and showed evidence of differentiation into multiple lineages in vitro. They also expressed low levels of pluripotency genes, OCT4, NANOG, SOX2 and KLF4. Passaging markedly affected cell proliferation with concomitant decreases in the expression of pluripotency and other markers, and an increase in chondrogenic markers. Microarray analysis further revealed the differences in the gene expression of CPJ-, CT- and WJ-hUC cells. Five coding and five lncRNA genes were differentially expressed in low vs. high passage hUC cells. Only MAEL was expressed at high levels in both low and high passage CPJ-hUC cells. They displayed a greater proliferation limit and a higher degree of multi-lineage differentiation in vitro and warrant further investigation to determine their full differentiation capacity, and therapeutic and regenerative medicine potential. 

Retracted: No

PubPeer comments:
 Control images in Figure 3D appear identical, with the top one rotated 180u00b0. *** Contrast enhanced ![file] , 
 An additional concern: two images in Figure 5G appear to overlap after adjusting the intensity. *** ![file] ,
Liposomes modified with cyclic RGD peptide for tumor targeting
Authors: Sanyog Jain
Vivek Mishra
Praveen K Dubey
S P Vyas
Sunil Mahor
Journal: Journal of Drug Targeting (2004)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Cyclic RGD peptide; Sterically stabilized liposomes; Angiogenic endothelial cells; Integrins; Targetability
Affiliations: Drug Delivery Research Laboratory, Department of Pharmaceutical Sciences, Dr. Harisngh Gour University, Sagar, India.

Abstract:  Cyclic RGD peptide anchored sterically stabilized liposomes (RGD-SL) were investigated for selective and preferential presentation of carrier contents at angiogenic endothelial cells overexpressing alphavbeta3 integrins on and around tumor tissue and thus for assessing their targetabilty. Liposomes were prepared using distearoylphosphatidylcholine (DSPC), cholesterol and distearoylphosphatidylethanolamine-polyethyleneglycol-RGD peptide conjugate (DSPE-PEG-RGD) in a molar ratio 56:39:5. The control RAD peptide anchored sterically stabilized liposomes (RAD-SL) and liposome with 5 mol% PEG (SL) without peptide conjugate which had similar lipid composition were used for comparison. The average size of all liposome preparations prepared was approximately 105 nm and maximum drug entrapment was 10.5+/- 1.1%. In vitro endothelial cell binding of liposomes exhibited 7-fold higher binding of RGD-SL to HUVEC in comparison to the SL and RAD-SL. Spontaneous lung metastasis and angiogenesis assays show that RGD peptide anchored liposomes are significantly (p&lt;0.01) effective in the prevention of lung metastasis and angiogenesis compared to free 5-FU, SL and RAD-SL. In therapeutic experiments, 5-FU, SL, RGD-SL and RAD-SL were administered intravenously on day 4 at the dose of 10 mg 5-FU/kg body weight to B16F10 tumor bearing BALB/c mice resulting in effective regression of tumors compared with free 5-FU, SL and RAD-SL. Results indicate that cyclic RGD peptide anchored sterically stabilized liposomes bearing 5-FU are significantly (p&lt;0.01) active against primary tumor and metastasis than the non-targeted sterically stabilized liposomes and free drug. Thus cyclic RGD peptide anchored sterically stabilized liposomes hold potential of targeted cancer chemotherapeutics. 

Retracted: No

PubPeer comments:
  FIGURE 6 Histopathological analysis (hematoxylin and eosin stain) of B16F10 tumors treated with: (a) SL and (b) RGD-SL  Here is 6(b), where I have marked some of the repeating elements. These do not encourage my faith in the veridicality of the image. ![file] , 
 #1 6(a) is more of the same. ![file] ,
Physcion induces apoptosis through triggering endoplasmic reticulum stress in hepatocellular carcinoma
Authors: Li-Hua Huang
Yan Li
Xiao-Ping Pan
Chen Wang
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: AMPK; ER stress; HCC; Key words; Physcion.
Affiliations: The People's Hospital of Wuhai, Wuhai, Inner Mongolia, China; Baotou Medical College, Baotou, Inner Mongolia, China. Electronic address: ., The People's Hospital of Wuhai, Wuhai, Inner Mongolia, China., Baotou Medical College, Baotou, Inner Mongolia, China. Electronic address: .

Abstract:  Hepatocellular carcinoma (HCC) is one of the most common and aggressive malignancies. The current study aimed to investigate the effect of physcion, a major active ingredient in several traditional herbal medicinal plants, for the treatment of HCC. Our data showed that physcion markedly induced apoptosis in human HCC cell lines Huh7 and Bel7402. The pro-apoptotic role of physcion on HCC cells was mediated by mitochondria dysfunction, which was caused by activation of endoplasmic reticulum(ER) stress. Moreover, our findings revealed that physcion stimulated ER stress by activating AMPK signaling. Besides in HCC cell lines, the anti-cancer activity of physcion was also examined in a xenograft mice model, which showed that physcion could significantly suppressed tumor growth. In conclusion, our results indicated that physcion can be considered as a potential chemotherapeutic agent in the treatment of HCC. 

Retracted: No

PubPeer comments:
 Fig 5 E,  Pretreatment with compound C (5 u03bcM) or knockdown of AMPK significantly abolished physcion-induced apoptosis . ![file] Left- and right-hand Huh-7 panels are very similar except for the extra clump of cell-points in the right-hand panel. Physcion Compound-C Huh-7 panel includes two identical clumps of cells (marked in blue). Bel-7402 Control panel is recognisable from [Yang et al (2019)] and [Liu et al (2019)] . ![] , 
 Below: Figs 2B ( Physcion induces apoptotic cell death in vivo ) and C ( Physcion improved the levels of cleaved caspase-3, cleaved caspase-12 and CHOP while decreases level of Ki-67 in vivo ). Above: Fig 7D,  Representative pictures of IHC staining for Ki-67, cleaved caspase-3, Bcl-2, Bax and RAD51 in the xenograft tumor tissues , from [Li et al (2019)] . ![file] ,
Use of rpoB Gene Analysis for Detection and Identification of Bartonella Species
Authors: D Raoult
M Drancourt
P Renesto
J Gouvernet
V Roux
Journal: Journal of Clinical Microbiology (2001)
Discipline: MICROBIOLOGY
Keywords: Bartonella species; RNA polymerase beta-subunit gene; PCR; PCR-RFLP analysis; clinical samples
Affiliations: Unité des Rickettsies, CNRS UPRES-A 6020, Faculté de Médecine, Université de la Méditerranée, 13385 Marseille, France., <!--label omitted: 2-->Service de l'Information Médicale, Hôpital de la Timone,2 13385 Marseille, France, <!--label omitted: 1-->Unité des Rickettsies, CNRS UPRES-A 6020, Faculté de Médecine, Université de la Méditerranée,1 and

Abstract:  Identification of Bartonella species is of increasing importance as the number of infections in which these bacteria are involved increases. To date, these gram-negative bacilli have been identified by various serological, biochemical, and genotypic methods. However, the development of alternative tools is required, principally to circumvent a major risk of contamination during sample manipulation. The aim of our study was to investigate the possible identification of various Bartonella species by comparison of RNA polymerase beta-subunit gene (rpoB) sequences. This approach has previously been shown to be useful for the identification of members of the family Enterobacteriaceae (C. M. Mollet, M. Drancourt, and D. Raoult, Mol. Microbiol. 26:1005-1011, 1997). Following PCR amplification with specific oligonucleotides, a 825-bp region of the rpoB gene was sequenced from 13 distinct Bartonella strains. Analysis of these sequences allowed selection of three restriction enzymes (ApoI, AluI, and AflIII) useful for discerning the different strains by PCR-restriction fragment length polymorphism (PCR-RFLP) analysis. To confirm the potential value of such an approach for identification of Bartonella, the rpoB PCR was then applied to 94 clinical samples, and the results obtained were identical to those obtained by our reference PCR method. Twenty-four isolates were also adequately identified by PCR-RFLP analysis. In all cases, our results were in accordance with those of the reference method. Moreover, conserved regions of DNA were chosen as suitable primer targets for PCR amplification of a 439-bp fragment which can be easily sequenced. 

Retracted: No

PubPeer comments:
 Figure 3 and 4. * Boxes of the same color show areas (some including bands) that look more similar to each other than expected. * Green boxes point to sharp background transitions. * The area above the bands in lanes 1-5 of Figure 4 also appears to show repetitiveness. Image made darker to bring out more features. This is probably a long shot, but would the authors happen to still have the original gel photos? ![file] ,
Resolvin D1 Modulates the Intracellular VEGF-Related miRNAs of Retinal Photoreceptors Challenged With High Glucose
Authors: Jorge Miquel Barcia
Claudio Bucolo
Marilena Galdiero
Giovanna Cuomo
Roberto Alfano
Anca Hermenean
Rosa Maisto
Sara Izzo
Maria Consiglia Trotta
Francesco Petrillo
Michele D&#x27;Amico
Chiara Bianca Maria Platania
Journal: Frontiers in pharmacology (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: VEGF; exosomes; miRNAs; resolvin D1; retinal photoreceptors.
Affiliations: Section of Pharmacology, Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy., Department of Experimental Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy., Multidisciplinary Department of Surgical and Dental Specialties, University of Campania "Luigi Vanvitelli", Naples, Italy., Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy., Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy., Institute of Life Sciences, Vasile Goldis Western University of Arad, Arad, Romania., School of Medicine, Catholic University of Valencia "Saint Vicente Martir", Valencia, Spain., Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, Catania, Italy.

Abstract:  Stimulation of retinal photoreceptors with elevated glucose concentration (30 mM) for 96 h, served as diabetic retinopathy in vitro model to study Resolvin D1 (50 nM) effects on neovascularization. VEGF and anti-angiogenic miR-20a-3p, miR-20a-5p, miR-106a-5p, and miR-20b expression was assessed either in photoreceptors exposed to HG or in exosomes released by those cells. High glucose increased VEGF levels and concurrently decreased anti-angiogenic miRNAs content in photoreceptors and exosomes. RvD1 reverted the effects of glucose damage in photoreceptors and exosomal pro-angiogenic potential, tested with the HUVEC angiogenesis assay. By activating FPR2 receptor, RvD1 modulated both the expression of anti-angiogenic miRNA, which decrease VEGF, and the pro-angiogenic potential of exosomes released by primary retinal cells. HUVEC transfection with miR-20a-3p, miR-20a-5p, miR-106a-5p, and miR-20b antagomirs, followed by exposure to exosomes from photoreceptors, confirmed the VEGF-related miRNAs mechanism and the anti-angiogenic effects of RvD1. 

Retracted: No

PubPeer comments:
 suspected figure manipulations![file] ![file] , 
 #1 We already provided an errata corrige of the manuscript. ,
miR-132 weakens proliferation and invasion of glioma cells via the inhibition of Gli1
Authors: S-Q Fan
G-M Xu
W Yang
Y-Z Wang
J-J Han
T-J Xu
Y-B Zhang
Journal: European Review for Medical and Pharmacological Sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Gli1; miR-132; proliferation; invasion; glioma
Affiliations: Department of Neurosurgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China. .

Abstract:  Objective: Transcriptional factor Gli1 in Hedgehog signal pathway facilitates epithelial mesenchymal transition (EMT) and is associated with invasion or proliferation of multiple tumor cells. The previous study showed the correlation between miR-132 down-regulation and glioma pathogenesis. We investigated the role of miR-132 in mediating Gli1 expression and in affecting proliferation or invasion of glioma cells. Patients and methods: Dual luciferase reporter gene assay was used to confirm the targeted regulation between miR-132 and Gli1. Tumor tissues at different pathological grades (grade II, III and IV) were collected from glioma patients, in parallel with brain tissues from contusion surgery. The expression of miR-132 and Gli1 was measured by RT-PCR. Glioma cell line U251 was treated with miR-132 or si-Gli1 followed by measuring the expression of Gli1, E-cadherin, Vimentin and Cyclin D1. In addition, flow cytometry and transwell assay were performed to evaluate cell invasion potency. Results: Bioinformatics analysis showed the complementary binding sites between miR-132 and 3'-UTR of Gli1 mRNA. Transfection of miR-132 mimic significantly reduced luciferase activity, indicating the targeted regulatory relationship between miR-132 and Gli1 mRNA. Compared with control group, miR-132 expression was decreased and Gli1 level was elevated in glioma tissues, both of which were correlated with the pathological grade. Transfection of miR-132 mimic or si-Gli1 remarkably suppressed the expression of Gli1, Vimentin or Cyclin D1 in U251 cells, up-regulated E-cadherin expression, suppressed cell proliferation and invasion. Conclusions: Our data indicated that over-expression of miR-132 could inhibit proliferation or invasion of glioma cells via targeted inhibition of Gli1 expression. 

Retracted: No

PubPeer comments:
 ![file] ![file] The Western Blots in this paper are sharp-edged black oval blobs on a featureless grey background. These are among the characteristics of [a papermill discussed here] , with examples listed in a Google document. https: docs.google.com spreadsheets d 1qBqQMXgzxoBd5bTbqdMuapGheupE5bdIopypju417NM edit#gid=0 ,
lncRNA HCG11 regulates cell progression by targeting miR‐543 and regulating AKT/mTOR pathway in prostate cancer
Authors: Yong-Liang Ma
Chun-Hui Dong
Long Pei
Wen-Yan He
Yan-Chao Wang
Journal: Cell Biology International (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: PI3K/AKT; cell growth; lncRNA HCG; miR-543; prostate cancer.
Affiliations: Department of Urology, the Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050011, China., Department of Urology, Yan'an People's Hospital, Yan'an, Shaanxi, 716000, China.

Abstract:  Prostate cancer (PCa) is a common cancer worldwide, which mostly occurs in males over the age of 50. Accumulating evidence have determined that long non-coding RNA/microRNA (lncRNA/miRNA) axis plays a critical role in cell progression of cancers, including PCa. However, the pathogenesis of PCa has not been fully indicated. In this study, quantitative real-time polymerase chain reaction was used to detect the expression of HCG11 and miR-543. Western blot was applied to measure the protein expression of proliferating cell nuclear antigen, cleavage-caspase 3 (cle-caspase 3), N-cadherin, E-cadherin, GAPDH, P-AKT, AKT, p-mTOR, and mTOR. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), transwell invasion, and transwell migration assay were used to detect cell proliferation, invasion, and migration, respectively. The function and mechanism of lncRNA HCG11 were confirmed in PCa cell and xenograft mice models. Luciferase assay indicated that miR-543 was a target miRNA of HCG11. Further investigation revealed that overexpression of HCG11 inhibited cell proliferation, invasion, and migration, whereas induced cell apoptosis by regulating miR-543 expression in vitro and in vivo. More than that, lncRNA HCG11 inhibited phosphoinositide-3 kinase/protein kinaseB (PI3K/AKT) signaling pathway to suppress PCa progression. Our data showed the overexpression of HGC11-inhibited PI3K/AKT signaling pathway by downregulating miR-543 expression, resulting in the suppression of cell growth in PCa. This finding proved a new regulatory network in PCa and provided a novel therapeutic target of PCa. 

Retracted: No

PubPeer comments:
 The Western immunoblots in this paper have an unusual appearance: all bands are blurry. They resemble several other blots seen in papers from different journals, which have been shown to origin from the so called papermills in China. The corresponding author, Yong-Liang Ma, has an email address which is not related to his name. This is also an indication that this paper originate from a papermill. Could the authors please provide raw data of the Western immunoblots (uncut membranes with Mw markers)? ![file] ,
Preparation of Calcipotriol Emulsion Using Bacterial Exopolysaccharides as Emulsifier for Percutaneous Treatment of Psoriasis Vulgaris
Authors: Hairong Chu
Ruiteng Song
Fang Yan
Min Cheng
Bo Song
Yuzhen Wang
Journal: International Journal of Molecular Sciences (2019)
Discipline: CHEMISTRY
Keywords: calcipotriol; emulsion; exopolysaccharides; psoriasis.
Affiliations: School of Pharmacy, Weifang Medical University, Weifang 261042, Shandong, China., Clinical Medical School, Weifang Medical University, Weifang 261042, Shandong, China.

Abstract:  An exopolysaccharides/calcipotriol (EPS/CPT) emulsion was prepared using bacterial EPS as emulsifier, sunflower oil as an oil phase and CPT as the loaded drug, and the effect of this emulsion on psoriasis vulgaris treatment was evaluated. An EPS composed of mannose (70.56%) and glucose (29.44%) was obtained from the marine mangrove bacteria Bacillus amyloliquefaciens ZWJ (Zhu Wenjing) strain. The EPS has significant emulsifying activity at the concentration of 1.5%. The prepared EPS/CPT emulsion has small and stable particle size, with a drug content of 0.00492%, and good spreading properties. The in vitro drug release results revealed that the emulsion showed a certain sustained release effect. In vitro and in vivo animal experiments show that the EPS/CPT emulsion can effectively treat psoriasis vulgaris by increasing the accumulation of CPT in psoriatic skin lesions and reducing the levels of inflammatory cells and inflammatory factors (TNF and IL6). Additionally, it has a certain effect on reducing the side effects associated with CPT. This study lays a foundation for the research of EPS in the topical application of medical materials and treatment of psoriasis. 

Retracted: No

PubPeer comments:
 The magnification, field of view and focus is different in each of the images present. If one focusses on any of the rows you can see that they are not the same magnification as the last panel of the overlay, even the magnification is off by quite a bit. ![file] , 
 #1 Thank you for your comment, the visible problems in the magnification, field of view and focus were inadvertently caused while assembling these figures in powerpoint prior to assembling in adobe where some part of the images got mistakenly over cropped and slightly stretched to resize with other panels. We sincerely apologize for this error. Nonetheless, there are enough common regions in all the image panels that show inverse expression of two proteins Runx2 and SKP2 in the indicated panels. Also, this inadvertent error does not change the conclusion because we also confirmed this inverse expression between these two proteins by immunoblotting in other panels of fig 6 with protein lysates from the same experiment as well as other settings too. Thanks for your interest in our finding. We shall be more careful in future. ,
Silencing of metallothionein-I gene in mouse lymphosarcoma cells by methylation
Authors: S Majumder
Y Bo
Z Li
S T Jacob
K Ghoshal
Journal: Oncogene (1999)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Metallothionein-I; gene silencing; methylation; CpG islands; lymphosarcoma
Affiliations: Department of Medical Biochemistry, College of Medicine, Ohio State University, Columbus 43210, USA.

Abstract:  Metallothionein-I (MT-I) gene is silenced by methylation of CpG islands in mouse lymphosarcoma P1798 cells but not in the thymus, the cell type from which the tumor was derived. Bisulfite genomic sequencing revealed that all 21 CpG dinucleotides present within -216 bp to +1 bp with respect to transcription start site are methylated in the tumor cell line, but none is methylated in the thymus. The lymphosarcoma cells induced MT-I in response to heavy metals only after demethylation with 5-azacytidine (5-AsaC). The electrophoretic mobility shift assay using specific oligonucleotide probes showed that the key transcription factors regulating MT-I gene (e.g., MTF-1, Sp 1 and MLTF/USF) are active in P1798 cells. In vivo footprinting of the proximal promoter region showed that none of the metal regulatory elements (MREs) or MLTF/USF are occupied in response to heavy metals. Demethylation of the lymphosarcoma cells with 5-AzaC resulted in constitutive footprinting at MLTF/ARE, and zinc-inducible footprinting at MRE-c, MRE-d and MRE-e sites. Demethylation of just 10-20% of the CpG islands was sufficient to render the gene inducible by cadmium or zinc. The MT-I induction persisted in the cancer cells for several generations even after withdrawal of 5-AzaC from the culture medium. 

Retracted: No

PubPeer comments:
null, 
 https: www.thelantern.com 2021 05 two-ohio-state-professors-lose-emeritus-titles-for-research-misconduct-sexual-harassment , 
 https: retractionwatch.com 2022 07 25 exclusive-osu-investigation-finds-dishonesty-and-permissive-culture-of-data-manipulation-in-cancer-research-lab ,
Monodisperse core/shell Ni/FePt nanoparticles and their conversion to Ni/Pt to catalyze oxygen reduction
Authors: Vicky V T Doan-Nguyen
Christopher B Murray
Yaoting Wu
Dong Su
Yizhou Hao
Shouheng Sun
Sen Zhang
Jing Li
Journal: Journal of the American Chemical Society (2014)
Discipline: CHEMISTRY
Keywords: core/shell nanoparticles; Ni/FePt; Ni/Pt; seed-mediated growth; surface oxidation
Affiliations: Department of Chemistry and ‡Department of Materials Science and Engineering, University of Pennsylvania , Philadelphia, Pennsylvania 19104, United States., Center
for Functional Nanomaterials, Brookhaven National Laboratory, Upton, New York 11973, United States, Department
of Chemistry, Brown University, Providence, Rhode Island 02912, United States

Abstract:  We report a size-controllable synthesis of monodisperse core/shell Ni/FePt nanoparticles (NPs) via a seed-mediated growth and their subsequent conversion to Ni/Pt NPs. Preventing surface oxidation of the Ni seeds is essential for the growth of uniform FePt shells. These Ni/FePt NPs have a thin (≈1 nm) FePt shell and can be converted to Ni/Pt by acetic acid wash to yield active catalysts for oxygen reduction reaction (ORR). Tuning the core size allows the optimization of their electrocatalytic activity. The specific activity and mass activity of 4.2/0.8 nm core/shell Ni/FePt after acetic acid wash reach 1.95 mA/cm(2) and 490 mA/mgPt at 0.9 V (vs reversible hydrogen electrode), which are much higher than those of benchmark commercial Pt catalyst (0.34 mA/cm(2) and 92 mA/mgPt at 0.9 V). Our studies provide a robust approach to monodisperse core/shell NPs with nonprecious metal core, making it possible to develop advanced NP catalysts with ultralow Pt content for ORR and many other heterogeneous reactions. 

Retracted: No

PubPeer comments:
 Can the author check the raw data to see how these similar noise patterns happened on the sample with without treatment? ![file] ,
α7 nicotinic acetylcholine receptor agonist attenuates the cerebral injury in a rat model of cardiopulmonary bypass by activating the Akt/GSK3β pathway
Authors: Tiezheng Zhang
Mei Wang
Keyan Chen
Yingjie Sun
Dandan Song
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: α7 nicotinic acetylcholine receptor; agonist; cerebral injuries; cardiopulmonary bypass; rats
Affiliations: Department of Anesthesiology, General Hospital of Shenyang Military Area Command, Shenyang, Liaoning 110016, P.R. China., Department of Laboratory Animal Science, China Medical University, Shenyang, Liaoning 110122, P.R. China.

Abstract:  α7 nicotinic acetylcholine receptor (α7nAchR) agonist treatment may provide a promising therapeutic effect for cerebral injuries. However, it is unclear whether the activation of α7nAchR agonist may reduce cerebral injuries induced by cardiopulmonary bypass (CPB). A total of 96 male Sprague‑Dawley rats were randomly divided into four groups (n=24/group): i) Sham operation group; ii) CPB group; iii) CPB + α7nAchR agonist group; and iv) CPB + α7nAchR agonist + α7nAchR antagonist group. Following treatment, 24 rats from each group were sacrificed and the serum and hippocampal tissues were collected. The serum expression levels of S100β, interleukin 6 and tumor necrosis factor α were evaluated by ELISA, hippocampal tissues were analyzed by histopathological examination using hematoxylin &amp; eosin and terminal deoxynucleotidyl‑transferase‑mediated dUTP nick‑end labeling (TUNEL) staining and Caspase 3 expression in the hippocampal tissues was evaluated by immunohistochemistry. In addition, Caspase 3, Akt and glycogen synthase kinase 3β (GSK3β), as well as phosphorylated (p)‑Akt and (p)‑GSK3β were examined by western blot assay. The present study demonstrated that α7nAchR agonist treatment was able to alleviate pathological damage and inhibit hippocampal cell apoptosis and inflammatory response. α7nAchR agonist treatment also increased the expression levels of p‑Akt and p‑GSK3β, which indicated an upregulation in Akt/GSK3β signaling. These data suggested that α7nAchR agonist may provide a promising new therapeutic approach for cerebral injury caused by CPB. 

Retracted: No

PubPeer comments:
 This paper has a 2010 Correction which corrects four sets of duplicated images. Three of these duplications were in Subhash C. Pandey et al. Journal of Neuroscience (2008), DOI: 10.1523 JNEUROSCI.4752-07.2008. See: https: pubpeer.com publications 9A4A142FE72EA5E58DFC0CA618D58C The duplication described in this Correction is as follows:  In Figure 5A of Pandey et al. (2006), the same photomicrograph was presented to document the placement of cannulae in aCSF- and BDNF antisense-treated subjects. Here is the original Figure 5A, which is now corrected, with the duplicated panels marked in pink. Of note, the circle marked  MeA in the center of both panels is not exactly drawn in the same position. ![file] ,
Diallyl disulfide suppresses proliferation and induces apoptosis in human gastric cancer through Wnt-1 signaling pathway by up-regulation of miR-200b and miR-22
Authors: Jiaoli Guo
Hailin Tang
Xinhua Xie
Xiaoming Xie
Lu Yang
Yanan Kong
Yi Tang
Qi Su
Journal: Cancer letters (2013)
Discipline: CLINICAL MEDICINE
Keywords: Diallyl disulfide; Gastric cancer; MicroRNA; Wnt-1 signaling pathway.
Affiliations: Department of Breast Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, People's Republic of China; State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, People's Republic of China; Cancer Research Institute, University of South China, Hengyang, Hunan, People's Republic of China.

Abstract:  The purpose of this study was to identify a mechanism related to miRNA pathway which plays a role in the anti-tumor effects of Diallyl disulfide. Alterations in miRNA expression were observed in Diallyl disulfide-treated MGC-803 cells, including up-regulation of miR-200b and miR-22 expression. Furthermore, Wnt-1 was identified as a target of both miR-200b and miR-22. MiR-200b and miR-22 not only synergistically inhibited gastric cancer growth, but also enhanced the antitumor effect of Diallyl disulfide both in vitro and in vivo. It indicated that miR-200b and miR-22 may serve as potential gene therapy and enhance Diallyl disulfide antitumor effects. 

Retracted: No

PubPeer comments:
 following up on a social media tip. There are several duplicated areas in panels of Figures 6 A and B. It is clear that the Wnt1 and TCF-4 panels for both the Scramble and and Mock samples are from the same parent image rather than representing different samples ![file] , 
 Large areas from different rows in the first column are identical ![file] , 
 #1 #2 Many thanks for identifying the similarities between these three figures. We have checked the original images of Figures 6 and we confirm that the images of the Wnt1 and TCF-4 group were mistakenly diplicated. We have contacted the editor for corrigendum. We do appreciate your identification of the mistake and the opportunity for us to realize and correct it. ,
LRRC19 expressed in the kidney induces TRAF2/6-mediated signals to prevent infection by uropathogenic bacteria
Authors: Hui Li
Shiyue Mei
Feifei Liu
Yongzhe Che
Xiaomin Su
Jia Yang
Wei Sun
Rongcun Yang
Limin Chai
Yining Zhao
Zhujun Zhang
Yuan Zhang
Hui Yan
Siping Min
Shuisong Cao
Journal: Nature Communications (2014)
Discipline: Multidisciplinary
Keywords: innate immune; bactericidal effects; urinary system; LRR; LRRC19
Affiliations: 1] Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China [2]., Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China., 1] Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China [2] Key Laboratory of Bioactive Materials Ministry of Education, Nankai University, Tianjin, China., 1] Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China [2] Key Laboratory of Bioactive Materials Ministry of Education, Nankai University, Tianjin, China [3] State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.

Abstract:  The innate immune-dependent bactericidal effects are critical for preventing microbial colonization in the urinary system. However, the mechanisms involved in establishing innate immune responses in kidney are not completely understood. Here we describe the role of a novel member of the LRR (leucine-rich repeat) class of transmembrane proteins, LRRC19 (LRR-containing 19) in eliminating uropathogenic bacteria. LRRC19 is predominantly expressed in human and mouse kidney tubular epithelial cells and LRRC19-deficient mice are more susceptible to uropathogenic Escherichia coli (UPEC) infection than wild-type or TLR4 knockout mice. Recognition of UPEC by LRRC19 induces the production of cytokines, chemokines and antimicrobial substances through TRAF2- and TRAF6-mediated NF-κB and MAPK signalling pathways. Thus, LRRC19 may be a critical pathogen-recognition receptor in kidney mediating the elimination of UPEC infection. 

Retracted: No

PubPeer comments:
 Could the authors explain the unexpected similarity between the values of WT vs the comparison group, figure 1 panel C: ![file] , 
 Also another concern about similarity of WT values across different tissues, same image: ![file] , 
 Here are exaplanations![file] ![file] ![file] , 
 ![file] ![file] Here are explanations.![file] , 
 Here are explanations![file] ![file] ![file] , 
 ![file] ,
Propranolol suppresses infantile hemangioma cell proliferation and promotes apoptosis by upregulating miR-125b expression
Authors: Shasha Zhao
Jiajia Huang
Aifeng Wang
Dongdong Jiang
Journal: Anti-Cancer Drugs (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Propranolol; infantile hemangioma; miR-125b; cell growth; apoptosis
Affiliations: Department of Pharmacy, Fuwai Central China Cardiovascular Hospital., College of Pharmacy, Zhengzhou University, Zhengzhou, People's Republic of China.

Abstract:  Propranolol could repress infantile hemangioma cell growth and induce apoptosis. miR-125b could inhibit cell proliferation in some tumors. However, whether propranolol exerts its proliferation inhibition and apoptosis-promoting effect by regulating the expression of miR-125b needs to be further investigated. In tumor tissue and endothelial cells isolated from infantile hemangioma patients, we found that the expression levels of miR-125b were significantly decreased. In-vitro analysis revealed that propranolol increased the expression of miR-125b in hemangioma cells in a dose-dependent and time-dependent manner. Interestingly, it was observed that regression of miR-125b expression by its inhibitor could abrogate the effect of propranolol on hemangioma cell growth and apoptosis. In addition, our data further identified TFAP4 as a direct target of miR-125b. Collectively, our data provided evidence that propranolol may repress infantile hemangioma cell growth and promote apoptosis through upregulating the miR-125b expression, which exerted its suppression of tumor development by targeting TFAP4. 

Retracted: Yes

PubPeer comments:
 Retracted, [April 2022] . The text of the retraction is only accessible to subscribers. In each flow-cytometry panel of Fig 3b, the stippled points form neat clouds centred within the quadrants . Points occasionally overlie the quadrant-division lines, which does not seem right for flow-cytometry. ![file] ,
Sequential ubiquitination of p53 by TRIM28, RLIM, and MDM2 in lung tumorigenesis
Authors: Dong Hoon Kang
Sang Hee Nam
Geun Dong Lee
Jae Kwang Yun
Tae Hyeong Lee
Jun-O Jin
Peter Chang-Whan Lee
Journal: Cell Death and Differentiation (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: TRIM28; E3 ubiquitin ligase; lung cancer; proliferation; migration
Affiliations: Shanghai Public Health Clinical Center, Shanghai Medical College, Fudan University, Shanghai, 201508, China., Department of Medical Biotechnology, Yeungnam University, Gyeongsan, 38541, Republic of Korea., Department of Thoracic and Cardiovascular Surgery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea., Lung Cancer Research Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea., Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea., Lung Cancer Research Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. ., Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea. .

Abstract:  Tripartite motif-containing 28 (TRIM28) is an E3 ubiquitin ligase harboring multiple cellular functions. We found that the TRIM28 protein is frequently overexpressed in patients with lung cancer. The stable overexpression of TRIM28 in lung cancer cells and xenograft models significantly increased the proliferation, migration, and invasiveness, whereas knockdown of TRIM28 had the opposite effect. We further observed that TRIM28 regulates the ubiquitin ligases RLIM and MDM2 to target the p53 levels during lung tumorigenesis. These data provide new insights into lung cancer development and potential new therapeutic targets for this disease. 

Retracted: No

PubPeer comments:
 The following blots in Figure 7C look similar (but should be from different samples): RLIM: 091719 and 092201 RLIM: 091612 and 69 ![file] , 
 ![file] ,
MicroRNA‑124 inhibits cell proliferation, invasion and migration by targeting CAV1 in bladder cancer
Authors: Yichuan Zhang
Leye He
Wandan Zhou
Bin Liu
Yinbo Dai
Jinrong Wang
Journal: Experimental and Therapeutic Medicine (2018)
Discipline: CLINICAL MEDICINE
Keywords: bladder cancer; caveolin 1; microRNA; tumour suppressor.
Affiliations: Department of Operation Center, Urology Group, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China., Department of Urology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, P.R. China.

Abstract:  MicroRNAs (miRs) may have promotive or suppressive roles in various human cancers types, but the molecular mechanisms underlying the role of miR-124 in bladder cancer (BC) progression have remained largely elusive. In the present study, it was observed that miR-124 was significantly downregulated in BC tissues compared with that in adjacent non-neoplastic tissues. Furthermore, its expression was also reduced in several human BC cell lines (T24, HT-1376 and 5637) compared with that in the normal bladder epithelial SV-HUC-1 cell line. A low expression of miR-124 in BC patients was significantly associated with advanced malignancy and a poor prognosis. Caveolin 1 (CAV1) was identified as a novel target gene of miR-124, and the expression of CAV1 was negatively regulated by miR-124 in T24 cells. Furthermore, CAV1 was identified to be significantly upregulated in BC tissues and cell lines, and a negative correlation was observed between the expression of miR-124 and CAV1 in BC tissues. Furthermore, restoration of miR-124 expression significantly inhibited the proliferation, migration and invasion of T24 cells, and these effects were impaired following overexpression of CAV1. Taken together, the present results demonstrate that miR-124 has a suppressive role in the proliferation, migration and invasion of BC cells by targeting CAV1, which suggests that miR-124 is a potential therapeutic candidate for BC. 

Retracted: Yes

PubPeer comments:
 Figs 5C, 6E. Transwell assays. ![file] Could the authors comment on the shared panels with Figs 2C, 3C, 7C of [Feng et al (2017)] ? ![file] And Figs 5C,D and 7A,B of [Li et al (2018)] ? ![file] , 
 Retracted [1 March 2022] .  Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that the Transwell cell migration assay data shown in Figs. 5C and 6E were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to *Experimental and Therapeutic Medicine*, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. ,
Cyclooxygenase-2 dependent metabolism of 20-HETE increases adiposity and adipocyte enlargement in mesenchymal stem cell-derived adipocytes
Authors: John R Falck
Joseph Shapiro
Dong Hyun Kim
Nitin Puri
Komal Sodhi
Michal L Schwartzman
Nader G Abraham
Journal: Journal of Lipid Research (2013)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: 20-HETE; adipogenesis; mesenchymal stem cells; COX; PPARγ
Affiliations: Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, USA.

Abstract:  20-Hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE), a product of the cytochrome P450 (CYP)-catalyzed ω-hydroxylation of arachidonic acid, induces oxidative stress and, in clinical studies, is associated with increased body mass index (BMI) and the metabolic syndrome. This study was designed to examine the effects of exogenous 20-HETE on mesenchymal stem cell (MSC)-derived adipocytes. The expression levels of CYP4A11 and CYP4F2 (major 20-HETE synthases in humans) in MSCs decreased during adipocyte differentiation; however, exogenous administration of 20-HETE (0.1-1 μM) increased adipogenesis in a dose-dependent manner in these cells (P &lt; 0.05). The inability of a 20-HETE analog to reproduce these effects suggested the involvement of a metabolic product of 20-HETE in mediating its pro-adipogenic effects. A cyclooxygenase (COX)-1 selective inhibitor enhanced, whereas a COX-2 selective or a dual COX-1/2 inhibitor attenuated adipogenesis induced by 20-HETE. The COX-derived metabolite of 20-HETE, 20-OH-PGE₂, enhanced adipogenesis and lipid accumulation in MSCs. The pro-adipogenic effects of 20-HETE and 20-OH-PGE₂ resulted in the increased expression of the adipogenic regulators PPARγ and β-catenin in MSC-derived adipocytes. Taken together we show for the first time that 20-HETE-derived COX-2-dependent 20-OH-PGE₂ enhances mature inflamed adipocyte hypertrophy in MSC undergoing adipogenic differentiation. 

Retracted: No

PubPeer comments:
 This actin control (figure 7 in this publicaton) now has been found in five papers (and counting?). The experiments differ with respect to the tissues examined (adipocytes vs. liver). In three cases animals were the source of tissue and in two case cultured cells were employed which includes this most recent discovery. In the present rendition the blot is associated with an experiment examining the effect of 20-Hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE) and cyclooxigenase inhibitors on the expression of adipocyte markers in adipocytes derived from human bone marrow mesenchymal stem cells (MSC) which is an entirely different experiment from the previous appearances. What follows is blot as it appeared in the figure from the paper and the actin blot aligned with the actin blots from the other papers. See also: https: pubpeer.com publications D0737900D02C1DD5D8721FB4B52372 ![file] ![file] ,
STAT1-p53-p21axis-dependent stress-induced progression of chronic nephrosis in adriamycin-induced mouse model
Authors: Zhaozhi Liang
Jiali Wang
Hua Wei
Journal: Annals of Translational Medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: Adriamycin; STAT1; chronic nephrosis (CN); mitogen-activated protein kinase; senescence.
Affiliations: Nephrology Department, Xinxiang Central Hospital, Xinxiang, China.

Abstract:  Background: Chronic nephrosis (CN) is an aging-related disease with high mortality. Signal transduction and transcriptional activator 1 (STAT1) protein promotes senescence in human glomerular mesangial cells (HMCs), but whether it affects the progression of adriamycin (ADR)-induced CN in vivo remains unclear. Methods: We established an ADR-induced CN mouse model that was completed in wild-type (wt) mice by a single intravenous injection of 10 mg/kg ADR for 2 or 4 weeks. Clinical indexes in each group were determined. Hematoxylin and eosin staining (H&amp;E) was employed to determine renal histopathological damage, SA-β-gal staining was used to evaluate cell senescence phenotype. TUNEL and immunohistochemistry (IHC) staining were used to detect renal apoptosis. Protein levels of Bcl-2, Bax, STAT1, p53 and p21 were measured by Western Blot. Results: STAT1 intervention ameliorated renal function. H&amp;E staining indicated that STAT1-deficient (stat1-/- ) improved the renal tubular injury, and stat1-/- obviously inhibited the apoptosis and Caspase-3+ number in kidney tissues. Besides, stat1-/- decreased proteinuria, and the levels of urea nitrogen and creatinine as well as that of reactive oxygen species induced by ADR. Also, stat1-/- resulted in the reduced expression of p53 and p21. Conclusions: Our current study strongly demonstrated the involvement of the STAT1-p53-p21 axis in the regulation of CN and is a potential target for the nephrosis treatment. 

Retracted: No

PubPeer comments:
 The abstract appears to be a product of [SCIgen] . * System administrators agree that scalable communication is an interesting new topic in the field of steganography, and leading analysts concur. After years of unfortunate research into context-free grammar, we argue the intuitive unification of fiber-optic cables and context-free grammar. Our focus here is not on whether sensor networks and randomized algorithms can collaborate to accomplish this aim, but rather on introducing an analysis of DHTs [2] (Soupy Coil). Found by the [Problematic Paper Screener] , a tool by by Guillaume Cabanac and Cyril Labbu00e9. ,