PReD-Bench/PRed-Bench huggingface dataset:
Role of DDX53 in taxol-resistance of cervix cancer cells in vitro
Authors: Jae Jun Lee
Sung Taek Park
Su Yeon Park
Jae Hwan Byun
Dooil Jeoung
Won Jin Kim
Youngmi Kim
Journal: Biochemical and Biophysical Research Communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Autophagy; Cervix cancer; DDX53; Drug-resistance.
Affiliations: Department of Obstetrics and Gynecology, Hallym University College of Medicine, Kangnam Sacred Heart Hospital, Seoul, South Korea., Department of Anesthesiology and Pain Medicine, College of Medicine, Hallym University, Chuncheon, South Korea., Department of Biochemistry, Kangwon National University, Chuncheon, South Korea., Institute of New Frontier Research, College of Medicine, Hallym University, Chuncheon, South Korea; Department of Anesthesiology and Pain Medicine, College of Medicine, Hallym University, Chuncheon, South Korea., Institute of New Frontier Research, College of Medicine, Hallym University, Chuncheon, South Korea; Department of Obstetrics and Gynecology, Hallym University College of Medicine, Kangnam Sacred Heart Hospital, Seoul, South Korea. Electronic address: ., Institute of New Frontier Research, College of Medicine, Hallym University, Chuncheon, South Korea. Electronic address: .

Abstract:  Cancer/Testis antigen DDX53 shows high expression level in various tumors and is involved in anti-cancer drug resistance. However, the functional study of DDX53 in cervix cancer remains unknown. In this study, the role of DDX53 in taxol-resistance of cervix cancer cells was investigated. In taxol-resistant HelaTR cells, DDX53 was significantly increased as compared to the parental HeLa cells. HelaTR cells also showed upregulation of multidrug resistant gene MDR1, invasive characteristics and decreased apoptosis. In addition, increased autophagy level was observed in HelaTR cells. Overexpression of DDX53 in HeLa and SiHa markedly led to greater resistance to taxol and cisplatin, whereas knockdown of DDX53 in HelaTR cells restored sensitivity, demonstrating that DDX53 regulated taxol resistance in cervix cancer cells. DDX53 overexpression in HeLa and SiHa cells enhanced invasion, migration and anchorage independent growth, DDX53 knockdown showed inverse effects in HeLaTR cells. When DDX53 expression was suppressed by siRNA, autophagic flux and drug resistance of HelaTR cells were decreased. In addition, DDX53 was upregulated in cervix cancer tissues from patient with a glassy cell carcinoma of cervix. Taken together, these results suggest that DDX53 plays a critical role in taxol-resistance by activating autophagy and a potential therapeutic target for the treatment of taxol-resistant cervix cancer. 

Retracted: No

PubPeer comments:
 Figures 2D and 3E appear to have an image which overlaps (cyan boxes), although the coloring and resolution seem different, suggesting this may not merely be an error during figure assembly. *** ![file] ,
Modification of the DNA damage response by therapeutic CDK4/6 inhibition
Authors: Erik S Knudsen
Jeffry L Dean
A Kathleen McClendon
Journal: Journal of Biological Chemistry (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: RB/E2F axis; cell signaling; gene transcription; DNA damage response; apoptosis signaling
Affiliations: Kimmel Cancer Center, Philadelphia, Pennsylvania, USA.

Abstract:  The RB/E2F axis represents a critical node of cell signaling that integrates a diverse array of signaling pathways. Recent evidence has suggested a role for E2F-mediated gene transcription in DNA damage response and repair, as well as apoptosis signaling. Herein, we investigated how repression of E2F activity via CDK4/6 inhibition and RB activation impacts the response of triple negative breast cancer (TNBC) to frequently used therapeutic agents. In combination with taxanes and anthracyclines CDK4/6 inhibition and consequent cell cycle arrest prevented the induction of DNA damage and associated cell death in an RB-dependent manner; thereby demonstrating antagonism between the cytostatic influence of the CDK-inhibitor and cytotoxic agents. As many of these effects were secondary to cell cycle arrest, γ-irradiation (IR) was utilized to examine effects of CDK4/6 inhibition on direct DNA damage. Although E2F controls a number of genes involved in DNA repair (e.g. Rad51), CDK4/6 inhibition did not alter the overall rate of DNA repair, rather it significantly shifted the burden of this repair from homologous recombination (HR) to non-homologous end joining (NHEJ). Together, these data indicate that CDK4/6 inhibition can antagonize cytotoxic therapeutic strategies and increases utilization of error-prone DNA repair mechanisms that could contribute to disease progression. 

Retracted: No

PubPeer comments:
 ![file] , 
 Thank you very much for pointing this out! We will bring it to the attention of the journal for a correction. ,
Downregulation of long non-coding RNA DBH-AS1 inhibits osteosarcoma progression by PI3K-AKT signaling pathways and indicates good prognosis
Authors: Z-B Liu
R-Q Lv
J-A Wang
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Long non-coding RNA; DBH-AS1; osteosarcoma; tumorigenesis; expression level
Affiliations: Clinical Laboratory, Songshan Hospital of Qingdao University Medical College, Qingdao, Shandong, China. .

Abstract:  Objective: Long non-coding RNA DBH-AS1 (DBH-AS1) has emerged as a novel regulator in cancer initiation and progression of several tumors. However, the expression of DBH-AS1 in osteosarcoma and its effect on the tumorigenesis of osteosarcoma are unclear. The purpose of this study was to determine the role of DBH-AS1 in osteosarcoma progression. Patients and methods: The expression level of DBH-AS1 in 119 pairs of osteosarcoma tissues and five cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The association of DBH-AS1 expression with clinicopathological factors and prognosis was also analyzed. Cell proliferation was measured by Cell Counting Kit-8 (CCK-8), EdU and cell colony formation assays and apoptosis in MG63 and U2OS cells was examined by flow cytometry. Following that, transwell invasion and wound-healing assays were used to explore cell migration and invasion, respectively. The expression of the PI3K/Akt pathway-related proteins was examined by Western blot analysis. Results: We observed that DBH-AS1 was distinctly overexpressed in osteosarcoma tissue and cells, and associated with lymph node status and metastasis status. Osteosarcoma patients with a higher DBH-AS1 expression showed significantly poorer overall survival than those with lower DBH-AS1 expression. Multivariate analysis demonstrated that high DBH-AS1 expression was an independent poor prognostic factor for osteosarcoma patients. Functional assays revealed that knockdown of DBH-AS1 inhibited cell proliferation, migration and invasion, while promoted apoptosis in osteosarcoma. Moreover, suppression of DBH-AS1 could inhibit the activation of the PI3K/Akt pathway, which was demonstrated by examining the expression levels of p-PI3K and p-Akt. Conclusions: Our data first reported that DBH-AS1 may act as an oncogenic lncRNA by modulating the PI3K/Akt pathway in osteosarcoma, which may serve as a candidate prognostic biomarker and target for new therapies in osteosarcoma. 

Retracted: No

PubPeer comments:
  Table III. Multivariate analysis of overall survival and disease-free survival in **ESCC** patients. ![file] The authors of this paper could not make up their minds whether they were studying osteosarcoma or esophageal squamous-cell carcinoma. Are the tabulated results for  overall survival or  disease-free survival ? ,
EMP3, which is regulated by miR-663a, suppresses gallbladder cancer progression via interference with the MAPK/ERK pathway
Authors: Lin Jiang
Fatao Liu
Shili Chen
Haibin Liang
Fei Zhang
Yunping Hu
Yingbin Liu
Maolan Li
Yijian Zhang
Yajuan Hao
Qiang Ma
Journal: Cancer Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: EMP3; Gallbladder cancer; MAPK/ERK; miR-663a.
Affiliations: Department of General Surgery, Xinhua Hospital Affiliated with Shanghai Jiao Tong University, School of Medicine, No. 1665 Kongjiang Road, Shanghai, 200092, China; Shanghai Key Laboratory of Biliary Tract Disease Research, No. 1665 Kongjiang Road, Shanghai, 200092, China. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor. Following the publication of the above article, the Editor was notified that images were duplicated in the migration and invasion experiments in Figures 3A, 6C, 7D and 8D: https://pubpeer.com/publications/76E82FD26E33503D7CCAC01C324AFA. The Editor has taken the decision to retract the paper as it is no longer acceptable in its current form 

Retracted: No

PubPeer comments:
 Could the authors examine the marked images from Figure 7D marked here in red (I believe that is the correct figure number)? They share unexpected similarities, *** ![file] , 
 #1 ![file] , 
 ![file] Figure 3A: ![file] , 
 More overlaps? *** 3A ![file] *** 8D ![file] *** 6C ![file] *** 7D ![file] , 
 Dear Dr. Biskrensis and Dr.Camphorifolia, Sorry for late reply. Thank you very much for your comments on our paper. We will take a look at our original data regarding the figure panels and respond to you as soon as possible. Many thanks again. Best regards Yingbin Liu , 
 #5 Is there any update on this? , 
 #6 Dear Dr. Biskrensis, thanks for your comments. We have already modified the figures and uploaded all the files to the editor for a corrigendum on April 2021. We contact with the editor actively all the time and process the corrigendum as the editor requires. We will tell you the final results at the first time. Thanks a lot Yingbin Liu , 
 Retracted [8 October 2022] .  This article has been retracted at the request of the Editor. Following the publication of the above article, the Editor was notified that images were duplicated in the migration and invasion experiments in Figures 3A, 6C and 7D and 8D: https: pubpeer.com publications 76E82FD26E33503D7CCAC01C324AFA. The Editor has taken the decision to retract the paper as it is no longer acceptable in its current form. ,
MC1R is dispensable for the proteinuria reducing and glomerular protective effect of melanocortin therapy
Authors: Pei Wang
Yan Ge
Anna-Lena Berg
Rujun Gong
Zhangsuo Liu
Sijie Zhou
Hai Wang
Songxia Quan
Yingjin Qiao
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: Melanocortin therapy; adrenocorticotropic hormone; proteinuria; glomerular injury; nephrotic syndrome
Affiliations: Institute of Nephrology, Blood Purification Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China., Division of Kidney Disease and Hypertension, Department of Medicine, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island, USA., Department of Nephrology, Lund University Hospital, Lund, Sweden., Department of Pathology, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island, USA.

Abstract:  Melanocortin therapy by using adrenocorticotropic hormone (ACTH) or non-steroidogenic melanocortin peptides attenuates proteinuria and glomerular injury in experimental glomerular diseases and induces remission of nephrotic syndrome in patients with diverse glomerulopathies, even those resistant to steroids. The underlying mechanism remains elusive, but the role of melanocortin 1 receptor (MC1R) has been implicated and was examined here. Four patients with congenital red hair color and nephrotic syndrome caused by idiopathic membranous nephropathy or focal segmental glomerulosclerosis were confirmed by gene sequencing to bear dominant-negative MC1R mutations. Despite prior corticosteroid resistance, all patients responded to ACTH monotherapy and ultimately achieved clinical remission, inferring a steroidogenic-independent and MC1R-dispensable anti-proteinuric effect of melanocortin signaling. In confirmatory animal studies, the protective effect of [Nle(4), D-Phe(7)]-α-melanocyte stimulating hormone (NDP-MSH), a potent non-steroidogenic pan-melanocortin receptor agonist, on the lipopolysaccharide elicited podocytopathy was completely preserved in MC1R-null mice, marked by reduced albuminuria and diminished histologic signs of podocyte injury. Moreover, in complementary in vitro studies, NDP-MSH attenuated the lipopolysaccharide elicited apoptosis, hypermotility and impairment of filtration barrier function equally in primary podocytes derived from MC1R-null and wild-type mice. Collectively, our findings suggest that melanocortin therapy confers a proteinuria reducing and podoprotective effect in proteinuric glomerulopathies via MC1R-independent mechanisms. 

Retracted: No

PubPeer comments:
 In Figure 2A, a Western blot has been duplicated and presented as something else. ![file] ,
Olax scandens Mediated Biogenic Synthesis of Ag-Cu Nanocomposites: Potential Against Inhibition of Drug-Resistant Microbes
Authors: Nuha Abeer Khan
Mohammad Owais
Ansam Wadia Faid Alshameri
Irfan Ghazi
Mohammad Kashif
Khan Farheen Badre Alam
Fauzia Jamal
Haris Saeed
Shadab Kazmi
Anzar Abdul Mujeeb
Journal: Frontiers in chemistry (2020)
Discipline: CHEMISTRY
Keywords: Ag-Cu NCs; anti-biofilm potential; antimicrobial potential; biogenic; reactive oxygen species (ROS).
Affiliations: Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh, India., Plant Molecular Biology and Genetic Engineering Division, The National Botanical Research Institute, Council of Scientific and Industrial Research, Lucknow, India., Department of Biochemistry, School of Life Sciences, University of Hyderabad, Hyderabad, India.

Abstract:  In the present study, we have synthesized silver-copper nanocomposites (Ag-Cu NCs) using an Olax scandens leaf extract (green synthesis method) and evaluated their antimicrobial potential against less susceptible pathogens. The kinetics of Ag-Cu NCs synthesis was followed by UV-VIS and fluorescence spectroscopy. The physicochemical characterization of as-synthesized Ag-Cu NCs was executed using electron microscopy, Energy Dispersive X-Ray, Fourier Transform Infrared Spectroscopy, and a Differential Light Scattering method. As-synthesized Ag-Cu NCs induced the formation of Reactive Oxygen Species (ROS), thereby causing alteration and decrementation of cellular proteins, DNA, lipids, etc., and eventually leading to cell death, as determined by a Live/Dead assay. Next, we assessed the anti-biofilm potential of as-synthesized Ag-Cu NCs against biofilm forming bacteria. The as-synthesized Ag-Cu NCs, when compared to monometallic silver nanoparticles, exhibited significantly higher anti-microbial activity against both sensitive as well as drug resistant microbial isolates. 

Retracted: No

PubPeer comments:
 Figure 5. * Red boxes: Panel A-C (Bacterial cells in presence of Ag-Cu NCs (62 ug ml)) looks very similar to panels B-A and B-C (Untreated bacterial cells (no NCs present)). Could the authors please clarify if these are expected to look so similar to each other? Maybe I am misunderstanding the legend, but it seems that these photos are representing different experimental conditions. ![file] , 
 Corrigendum, September 2020: https: www.frontiersin.org articles 10.3389 fchem.2020.00822 full  In the original article, there was a mistake in Figure 5A as published. An incorrect image was used in panel C. The corrected Figure 5A appears below. There was also a mistake in the legend for Figure 5 as published. The correct legend appears below. The authors apologize for these errors and state that they do not change the scientific conclusions of the article in any way. The original article has been updated. ,
Stac3 inhibits myoblast differentiation into myotubes
Authors: Sungwon Park
Xiaofei Cong
David E Gerrard
Xiaomei Ge
Honglin Jiang
Yafei Zhang
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: Stac3; myoblast proliferation; myoblast differentiation; skeletal muscle development; myotubes
Affiliations: Department of Animal and Poultry Sciences, Virginia Tech, Blacksburg, Virginia, United States of America.

Abstract:  The functionally undefined Stac3 gene, predicted to encode a SH3 domain- and C1 domain-containing protein, was recently found to be specifically expressed in skeletal muscle and essential to normal skeletal muscle development and contraction. In this study we determined the potential role of Stac3 in myoblast proliferation and differentiation, two important steps of muscle development. Neither siRNA-mediated Stac3 knockdown nor plasmid-mediated Stac3 overexpression affected the proliferation of C2C12 myoblasts. Stac3 knockdown promoted the differentiation of C2C12 myoblasts into myotubes as evidenced by increased fusion index, increased number of nuclei per myotube, and increased mRNA and protein expression of myogenic markers including myogenin and myosin heavy chain. In contrast, Stac3 overexpression inhibited the differentiation of C2C12 myoblasts into myotubes as evidenced by decreased fusion index, decreased number of nuclei per myotube, and decreased mRNA and protein expression of myogenic markers. Compared to wild-type myoblasts, myoblasts from Stac3 knockout mouse embryos showed accelerated differentiation into myotubes in culture as evidenced by increased fusion index, increased number of nuclei per myotube, and increased mRNA expression of myogenic markers. Collectively, these data suggest an inhibitory role of endogenous Stac3 in myoblast differentiation. Myogenesis is a tightly controlled program; myofibers formed from prematurely differentiated myoblasts are dysfunctional. Thus, Stac3 may play a role in preventing precocious myoblast differentiation during skeletal muscle development. 

Retracted: No

PubPeer comments:
 August 2014 correction found here: https: journals.plos.org plosone article?id=10.1371 journal.pone.0105240 It reads:  *There are errors in Figure 2. Please see the corrected Figure 2 here. * The correction does not specify the errors in the original figure 2. In May 2014, I reported a duplication between two panels, marked here with red boxes. That duplication is now corrected, for which I thank the authors. However, I just noticed another possible duplication, marked here by me with green boxes. That duplication is still present in the corrected figure. Could the authors please check? ![file] , 
 #1 I am the corresponding author of this paper, and I take Dr. Biku2019s concern seriously. Please let me check with the person who prepared this figure first. ,
Renoprotective Effects of AVE0991, a Nonpeptide Mas Receptor Agonist, in Experimental Acute Renal Injury
Authors: Mauro Martins Teixeira
Kátia Daniela Silveira
Milene Rachid
Valdinéria Borges
Cristiano Xavier Lima
Lívia Corrêa Barroso
Michael Bader
Danielle Gloria Souza
Ana Cristina Simões E Silva
Robson Augusto Souza Santos
Journal: International Journal of Hypertension (2012)
Discipline: CLINICAL MEDICINE
Keywords: Renal ischemia; reperfusion; acute kidney injury; leukocytes; inflammatory mediators
Affiliations: Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, UFMG, 31270-901 Belo Horizonte, MG, Brazil., Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, UFMG, 31270-901 Belo Horizonte, MG, Brazil, Departamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas, UFMG, 31270-901 Belo Horizonte, MG, Brazil, Departamento de Cirurgia, Faculdade de Medicina, UFMG, 30130-100 Belo Horizonte, MG, Brazil, Max Delbrück Center for Molecular Medicine, Berlin Buch, 13092 Berlin, Germany, Departamento de Patologia Geral, Instituto de Ciências Biológicas, UFMG, 31270-901 Belo Horizonte, MG, Brazil, Departamento de Microbiologia, Instituto de Ciências Biológicas, UFMG, 31270-901 Belo Horizonte, MG, Brazil, Departamento de Pediatria, Faculdade de Medicina, UFMG, 30130-100 Belo Horizonte, MG, Brazil

Abstract:  Renal ischemia and reperfusion (I/R) is the major cause of acute kidney injury in hospitalized patients. Mechanisms underlying reperfusion-associated injury include recruitment and activation of leukocytes and release of inflammatory mediators. In this study, we investigated the renal effects of acute administration of AVE0991, an agonist of Mas, the angiotensin-(1-7) receptor, the angiotensin-(1-7) receptor, in a murine model of renal I/R. Male C57BL/6 wild-type or Mas(-/-) mice were subjected to 30 min of bilateral ischemia and 24 h of reperfusion. Administration of AVE0991 promoted renoprotective effects, as seen by improvement of function, decreased tissue injury, prevention of local and remote leucocyte infiltration, and release of the chemokine, CXCL1. I/R injury was similar in WT and Mas(-/-) mice, suggesting that endogenous activation of this receptor does not control renal damage under baseline conditions. In conclusion, pharmacological interventions using Mas receptor agonists may represent a therapeutic opportunity for the treatment of renal I/R injury. 

Retracted: No

PubPeer comments:
 image duplications not referenced ![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. ,
miR-155 promotes the growth of osteosarcoma in a HBP1-dependent mechanism
Authors: Xiaohui Sun
Ying Liu
Hongxing Zhao
Xiaolin Geng
Jun Zhang
Journal: Molecular and Cellular Biochemistry (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Osteosarcoma; miR-155; proliferation; cell cycle progression; Wnt pathway
Affiliations: The Department of Orthopedics, The First Affiliated Hospital of Xinxiang Medical University, 88 Jiankang Road, Weihui, 453100, China, .

Abstract:  Osteosarcoma (OS) is a type of malignant tumor arising from soft-tissues of bone and displays poor prognosis in most cases. However, the molecular mechanism by which OS initiates and progresses is still not completely elucidated. miR-155 has been shown to be overexpressed in OS specimen and cell lines. Our study is intended to explore the role of miR-155 in OS etiology. The data confirmed that miR-155 abundance is higher in OS samples than non-cancerous bone tissue. Inhibition of miR-155 suppressed the proliferation of OS cells and cell cycle progression in vitro, and the growth of OS xenografts in vivo. Wnt pathway was suppressed in OS cells by miR-155 inhibitors. HMG-box transcription factor 1 (HBP1), a strong Wnt pathway suppressor, was found to be a target of miR-155. Restoration of HBP1 abolished the effect of miR-155 on OS cells. Finally, miR-155 levels in OS tissues and serum are both inversely associated with the survival of OS patients. Collectively, miR-155 was identified to be among the list of OS-related oncogenic miRNAs, and HBP1-mediated Wnt signaling is involved with the role of miR-155 in OS progression. 

Retracted: No

PubPeer comments:
 Western Blot bands appear in multiple papers from non-overlapping teams of authors. *[left]* Figs 5B,C.  The expression level of HBP1 was detected by immunoblot analysis in U2OS and SaOS2 cells treated with miR-155 inhibitor ;  The expression level of HBP1 was detected by immunoblot analysis in hFOB1.19 and HEK293 cells transfected with miR-155 mimics . *[right]* Fig 7A from [Hong et al (2015)] .  A549 cells were infected with Ad-piR-55490 or and Ad-mTOR (10 MOI) as well as Ad-EGFP (10 MOI), and 48 h later, immunoblot analysis was performed to detect mTOR expression level . Violet boxes mark a loading control that is either GAPDH or beta-tubulin. ![file] Rose box invites comparisons with *[left]* Fig 5a of [Peng et al (2016)] and *[right]* Fig 2a from [Song et al (2016)] . ![] UPDATE: Another sighting of the rose-boxed band! *[left]* Fig 5E from [Zhang, Zhang Li (2015)] .  MEF2D protein was examined by immunoblotting in A549 and H460 cells under such treatments . *[right]* Fig 4B from [Hong et al (2015)] .  Western blot assay was conducted to confirm the above results . ![file] ,
Osteoinductive effects of tantalum and titanium on bone mesenchymal stromal cells and bone formation in ovariectomized rats
Authors: D Zou
P-S Wu
H-L Cao
M-M Lu
X-J Guo
L-L Yin
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Tantalum; Titanium; Osteoporosis; Osteoinductivity; Bone mesenchymal stromal cells
Affiliations: Department of Stomatology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China. .

Abstract:  Objective: Although Tantalum (Ta) exhibits better osteoinductivity in healthy subjects when compared with titanium (Ti), the relative effects in osteoporosis remain unknown. Materials and methods: In this study, bone mesenchymal stromal cells of ovariectomized rats (OVX-rBMSCs) were seeded on Ta and Ti substrates for in vitro evaluation of cell viability, reactive oxygen species (ROS) production, alkaline phosphatase (ALP) activity, extracellular mineralization osteogenic gene and protein expression involved in bone morphogenetic protein (BMP2)/small mothers against decapentaplegic homologs 1 (Smad1) pathway. For in vivo assessment, Ta and Ti implants were embedded in femur defects of ovariectomized rats, followed by sequential fluorochrome labeling and histological staining. Results: Compared to Ti, the Ta substrates demonstrated higher viable cell percentages (96.5 ± 0.26 vs. 88.17 ± 2.23%), lower ROS levels (65% vs. Ti), and enhanced ALP activity and extracellular matrix calcification. Reverse Transcription-Polymerase Chain Reaction and Western blot assays validated the better osteoinductive effect of Ta regarding small mothers against decapentaplegic homologs 1 (Smad1), runt-related transcription factor 2, bone morphogenetic protein (BMP2), and ALP expression at both the mRNA (1.5-2-fold) and protein (1.2-1.8-fold) levels. BMP2/Smad1 signaling over-expression or knockdown yielded significantly enhanced or deteriorated OVX-rBMSC osteogenesis on the two surfaces. In addition, the Ta group revealed more new bone formation (1.3-1.5-fold vs. Ti) and slightly better bone-implant contact (31.82 ± 4.07 vs. 25.2-3.84% at 8 weeks post-implantation, p = 0.052) without the contribution of specific surface structures. Conclusions: In comparison to Ti, Ta reveals better biocompatibility and osteoinductivity to OVX-rBMSCs, and the preferential Ta osteoinductivity may reflect its greater potential to trigger the BMP2/Smad1 cascade. Thus," in front of "Ta". Ta appears preferable to Ti as a bone-implant surface material under osteoporosis conditions. 

Retracted: No

PubPeer comments:
 Figure 2A. * Rounded boxes of the same color focus attention to unexpectedly similar areas across panels ![file] ,
Retraction : lncRNA CCAT1 contributes to the growth and invasion of gastric cancer via targeting miR‐219‐1
Authors: Yanfeng Li
Hongyan Qu
Yan Ma
Guanyu Zhu
Journal: Journal of Cellular Biochemistry (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: apoptosis; gastric cancer; invasion; lncRNA CCAT1; miR-219-1
Affiliations: Department of Gastrointestinal Surgery, the Affiliated Cancer Hospital of Harbin Medical University, Harbin, Heilongjiang, 150040, China.

Abstract:  Gastric cancer (GC) is one of the most malignant tumors that seriously threaten to human health. Increased reports indicated that long non-coding RNAs (lncRNAs) were associated with GC. This study aims to investigate the regulatory role of colon cancer associated transcript-1 (CCAT1) in GC. The results exhibited that CCAT1 was higher expressed in 57 GC tissue samples than in 57 paired adjacent normal tissue samples. The expression of CCAT1 was also increased in GC cell lines (MKN45, Hs746T and SGC-7901) compared with gastric epithelial cell line GES-1. Besides, decreased cell proliferation with increased cell apoptosis were detected in SGC-7902 cells transfected with CCAT1 shRNA. At the same time, lower cell invasion ability was measured in SCG-7901 cells transfected with CCAT1-shRNA. In addition, miR-219-1 was predicted and convinced a direct target of CCAT1. The expression of miR-219-1 was declined in GC tissues and GC cell lines. Further studies demonstrated that the roles of CCAT1 on cell proliferation, apoptosis and invasion were inhibited by miR-219-1. At last, the in vivo experiment indicated that tumor growth of GC was suppressed through knockdown of CCAT1. In conclusion, these results suggested that CAT1 promotes the tumorigenesis and progression of GC by negative-regulating miR-219-1. This article is protected by copyright. All rights reserved. 

Retracted: No

PubPeer comments:
  lncRNA CCAT1 contributes to the growth and invasion of gastric cancer via targeting miRu2010219u20101u201d by Yanfeng Li, Guanyu Zhu, Yan Ma, and Hongyan Qu published online on 12 December 2017 in Wiley Online Library (wileyonlinelibrary.com), has been withdrawn by agreement between the journal Editor in Chief Gary S. Stein and John Wiley and Sons, Inc. The retraction has been agreed because the authors are not responding to requests to finalize their article for publication in the journal as the Version of Record. Subsequently this paper was resubmitted, and this time successfully published. Its problematic images are discussed in the [PP thread appropriate to that second version] . ![] ![] ,
Tricin, flavonoid from Njavara reduces inflammatory responses in hPBMCs by modulating the p38MAPK and PI3K/Akt pathways and prevents inflammation associated endothelial dysfunction in HUVECs
Authors: Jayalekshmy A
Sindhu G
Helen A
V Shalini
Chithra K Pushpan
Journal: Immunobiology (2016)
Discipline: IMMUNOLOGY
Keywords: Flavonoid; Inflammation; Lipopolysaccharide; Signaling; Tricin.
Affiliations: Department of Biochemistry, University of Kerala, Kariavattom Campus, Thiruvananthpuram, 695581 Kerala, India. Electronic address: ., Department of Biochemistry, University of Kerala, Kariavattom Campus, Thiruvananthpuram, 695581 Kerala, India., Chemical Sciences & Technology Division, National Institute for Interdisciplinary Science and Technology (NIIST), CSIR, Industrial Estate P.O., Thiruvananthapuram, 695019 Kerala, India. Electronic address: .

Abstract:  Previous studies revealed the potent anti-inflammatory activity of tricin, the active component of Njavara rice bran. Here, we report the involvement of specific signaling pathways in the protective effect of tricin against LPS induced inflammation in hPBMCs and the role of tricin in modulating endothelial dysfunction in LPS induced HUVECs. Pretreatment with tricin (15μM) significantly inhibited the release of TNF-α and was comparable to the specific pathway blockers like ERK inhibitor (PD98059), JNK inhibitor (SP600125) and p38 inhibitor (SB203580), whereas an increased release of TNF-α was observed in PI3K/Akt inhibitor (LY294002) treated cells. Tricin alone and combination treatment of tricin and SB203580 showed more significant inhibition of activation of COX-2 and TNF-α than that of SB203580 alone treated group. Combination treatment of tricin and LY294002 showed increased activation of COX-2 and TNF-α, proved that PI3K activation is essential for the anti-inflammatory effect of tricin. Studies conducted on HUVECs revealed the protective effect of tricin against endothelial dysfunction associated with LPS induced inflammation by inhibiting the activation of proinflammatory mediators like TNF-α, IFN-γ, MCP 1 by modulating NF-κB and MAPK signaling pathways. ELISA and flow cytometric analysis again confirmed the protection of tricin against endothelial damage, especially from the decreased activation of cell adhesion molecules like ICAM-1, VCAM-1 and E-Selectin upon tricin treatment. This work establishes the mechanism behind the potent anti-inflammatory activity of the flavonoid tricin. 

Retracted: No

PubPeer comments:
 The Fig 2B and Fig 3B have some unusual similarities. Figure 2B and 3B shows treatment with SB203580 and LY294002 respectively. The upper lanes of both 2B and 3B are cropped images and were reused (yellow). The b-actin is intact in both Fig 2B and 3B, stating different treatment condition (Red). The graphs were also found to be similar, though the y-axis of Fig. 3B is extended a bit (Green). Could the authors clarify this with their uncropped raw data. ![file] ,
Effect of miR-363 on the proliferation, invasion and apoptosis of laryngeal cancer by targeting Mcl-1
Authors: L-L Zhou
Y Sun
X-M Zhong
H Liu
L-J Xu
R Yao
W-T Feng
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miR-363; laryngeal cancer; Mcl-1; cell proliferation; invasion
Affiliations: Department of Oncology, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, China. .

Abstract:  Objective: To investigate the potential effect of miR-363 on the development of laryngeal cancer and to reveal the relevant mechanism. Patients and methods: The expression level of miR-363 was detected in laryngeal cancer tissues and cells (TU-177), respectively. Luciferase assay was performed to evaluate the interaction between miR-363 and myeloid cell leukemia-1 (Mcl-1). The effect of the miR-363/Mcl-1 axis on TU-177 cells was determined by subsequent experiments including cell proliferation, invasion, apoptosis and the expression level of Mcl-1. Results: In the present study, we found that miR-363 was both repressed in laryngeal cancer tissues and cells (TU-177). To find the regulating target of miR-363, we searched three publicly available algorithms, including TargetScan, miRDB, and microRNA. Results showed that Mcl-1 was a direct target of miR-363, and the Luciferase assay confirmed our suggestion. Subsequent experiments indicated that the decreased expression of Mcl-1 resulting from the up-regulation of miR-363 could deaccelerate cell proliferation and invasion, and accelerate cell apoptosis in laryngeal cancer cells. Conclusions: Our research revealed the suppressed function of miR-363 in laryngeal cancer by targeting Mcl-1. Meanwhile, we found that the restoration of miR-363 could serve as a potential therapeutic strategy for the treatment of laryngeal cancer. 

Retracted: No

PubPeer comments:
 The invasion transwell assay in Figure 4A appears to contain two images which overlap, with 180 degree rotation. Area of overlap marked roughly with red boxes. *** ![file] *** Full figure ![file] ,
Riluzole-triggered GSH synthesis via activation of glutamate transporters to antagonize methylmercury-induced oxidative stress in rat cerebral cortex
Authors: Bin Xu
Yan-Gang Wei
Hai-Bo Yang
Yu Deng
Zhao-Fa Xu
Wei Liu
Journal: Oxidative medicine and cellular longevity (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: riluzole; methylmercury; oxidative stress; glutathione synthesis; glutamate transporters
Affiliations: Department of Enviromental Health, School of Public Health, China Medical University, Liaoning, Shenyang 110001, China., Department of Enviromental Health, School of Public Health, China Medical University, Liaoning, Shenyang 110001, China

Abstract:  Objective: This study was to evaluate the effect of riluzole on methylmercury- (MeHg-) induced oxidative stress, through promotion of glutathione (GSH) synthesis by activating of glutamate transporters (GluTs) in rat cerebral cortex. Methods: Eighty rats were randomly assigned to four groups, control group, riluzole alone group, MeHg alone group, and riluzole + MeHg group. The neurotoxicity of MeHg was observed by measuring mercury (Hg) absorption, pathological changes, and cell apoptosis of cortex. Oxidative stress was evaluated via determining reactive oxygen species (ROS), 8-hydroxy-2-deoxyguanosine (8-OHdG), malondialdehyde (MDAs), carbonyl, sulfydryl, and GSH in cortex. Glutamate (Glu) transport was studied by measuring Glu, glutamine (Gln), mRNA, and protein of glutamate/aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1). Result: (1) MeHg induced Hg accumulation, pathological injury, and apoptosis of cortex; (2) MeHg increased ROS, 8-OHdG, MDA, and carbonyl, and inhibited sulfydryl and GSH; (3) MeHg elevated Glu, decreased Gln, and downregulated GLAST and GLT-1 mRNA expression and protein levels; (4) riluzole antagonized MeHg-induced downregulation of GLAST and GLT-1 function and expression, GSH depletion, oxidative stress, pathological injury, and apoptosis obviously. Conclusion: Data indicate that MeHg administration induced oxidative stress in cortex and that riluzole could antagonize this situation through elevation of GSH synthesis by activating of GluTs. 

Retracted: No

PubPeer comments:
 Two images in Figure 1 appear to overlap. 1c and 1d omitted. *** ![file] ![file] , 
 In addition to the concern within the figure above, there appears to be overlap between images in two different papers. Thread for the other paper https: pubpeer.com publications F727B801E9A5101814BD1430ED1D3C *** ![file] ,
Epidemiological Perspectives of Diabetes
Authors: Jing Zhao
Aimin Shi
Ziqi Tao
Journal: Cell Biochemistry and Biophysics (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Diabetes; Diagnosis; Epidemiological perspective.
Affiliations: Department of Science and Education, Xuzhou Central Hospital, No. 199 JieFang south Road, Xuzhou, 221009, Jiangsu, China. ., School of Public Health of Nanjing Medical University, Nanjing, 211166, Jiangsu, China., Department of Science and Education, Xuzhou Central Hospital, No. 199 JieFang south Road, Xuzhou, 221009, Jiangsu, China.

Abstract:  The global statistics of diabetes mellitus in year 2013 indicated, about 382 million people had this disease worldwide, with type 2 diabetes making up about 90 % of the cases. This is equal to 8.3 % of the adult population with equal rates in both women and men. In year 2012 and 2013 diabetes resulted in mortality of 1.5-5.1 million people per year, making it the 8th leading cause of death in the world. It is predicted that by year 2035 about 592 million people will die of diabetes. The economic cost of diabetes seems to have increased worldwide. An average age of onset of diabetes is 42.5 years and could be due to consumption of high sugar and high-calorie diet, low physical activity, genetic susceptibility, and lifestyle. Approximately 8 % children and about 26 % young adults have diabetes mellitus in the world. The results of epidemiological study of type 1 diabetes mellitus (T1D) are presented by demographic, geographic, biologic, cultural, and other factors in human populations. The prevalence of T1D has been increased by 2-5 % worldwide and its prevalence is approximately one in 300 in US by 18 years of age. The epidemiological studies are important to study the role, causes, clinical care, prevention, and treatment of type1 diabetes in pregnant women and their children before and after birth. In this article, causes, diagnosis, symptoms, treatment and medications, and epidemiology of diabetes will be described. 

Retracted: No

PubPeer comments:
 *[left]* The Introduction. *[right]* The introduction of the Wikipedia entry on Diabetes [(January 2015 version)] . Compared with [Simtexter] . ![file] ,
Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents
Authors: Cristin E Kearns
Laura A Schmidt
Stanton A Glantz
Journal: JAMA internal medicine (2016)
Discipline: CLINICAL MEDICINE
Keywords: coronary heart disease; sugar research foundation; dietary causes; sucrose consumption; CHD risk
Affiliations: Philip R. Lee Institute for Health Policy Studies, San Francisco, California2Department of Orofacial Sciences, University of California, San Francisco, San Francisco., Philip R. Lee Institute for Health Policy Studies, San Francisco, California3Clinical and Translational Science Institute, San Francisco, California4Department of Anthropology, History, and Social Medicine, University of California, San Francisco., Philip R. Lee Institute for Health Policy Studies, San Francisco, California5Department of Medicine, University of California, San Francisco, San Francisco6Center for Tobacco Control Research and Education, San Francisco, California7Cardiovascular Research Institute, San Francisco, California8Helen Diller Family Comprehensive Cancer Center, San Francisco, California.

Abstract:  Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents, historical reports, and statements relevant to early debates about the dietary causes of CHD and assembled findings chronologically into a narrative case study. The SRF sponsored its first CHD research project in 1965, a literature review published in the New England Journal of Medicine, which singled out fat and cholesterol as the dietary causes of CHD and downplayed evidence that sucrose consumption was also a risk factor. The SRF set the review's objective, contributed articles for inclusion, and received drafts. The SRF's funding and role was not disclosed. Together with other recent analyses of sugar industry documents, our findings suggest the industry sponsored a research program in the 1960s and 1970s that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in CHD. Policymaking committees should consider giving less weight to food industry-funded studies and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development. 

Retracted: No

PubPeer comments:
 A possible overlap between a panel in Figure 5D and one in Figure 5F was pointed out to me by a reader. Marked with red boxes: ![file] , 
 #1 We appreciate your valuable comment. By rechecking the original data, the first author Danni Deng found that he made the low-level mistake as you indicated, when selecting representative images from countless image data. We apologize for it! We will contact the journal and submit a corrigendum. ,
GM1 Induced the inflammatory response related to the Raf-1/MEK1/2/ERK1/2 pathway in co-culture of pig mesenchymal stem cells with RAW264.7
Authors: You Na Seo
Dong Hoon Kwak
Young Ho Cho
Soon Ju Park
Sun-Uk Kim
Young-Kug Choo
Ju Hyoung Lee
Ji-Su Kim
Journal: Animal Cells and Systems (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: GM1; MAPK; inflammation; pig-mesenchymal stem cells; xenotransplantation.
Affiliations: Institute of Glycosciences, Wonkwang University, Iksan, Republic of Korea., Institute of Aribio, Sungnam, Republic of Korea., Department of Biological Science, College of Natural Sciences, Wonkwang University, Iksan, Republic of Korea., Department of Pharmaceutics and Biotechnology, Medical Engineering College, Konyang University, Daejeon, Republic of Korea., National Primate Research Center, Korea Institute of Bioscience and Biotechnology, Cheongju, Republic of Korea.

Abstract:  Pig-human xenotransplantation can trigger cell-mediated immune responses. We explored the role of gangliosides in inflammation related to immune rejection in xenotransplantation. Co-culture of xenogeneic cells (pig-MSCs and RAW264.7) was used to emulate xenotransplantation conditions. MTT assay results indicated that cell viability was significantly decreased in pADMSCs co-cultured with RAW264.7 cells. GM1 and GM3 were highly expressed in pADMSCs co-cultured with RAW264.7 cells. pADMSCs co-cultured with RAW264.7 cells strongly expressed pro-inflammatory proteins such as COX-2, iNOS, p50, p65, pIκBα, and TNF-α. GM1-knockdown pADMSCs co-cultured with RAW 264.7 cells did not show significantly altered cell viability, but pro-inflammatory proteins were markedly inhibited. Co-culture of pADMSCs with RAW264.7 cells induced significant phosphorylation (p) of JNK1/2 and pERK1/2. However, pERK1/2 and pJNK1/2 were decreased and MEK1/2 and Raf1 were suppressed in GM1-knockdown pADMSCs co-cultured with RAW264.7 cells. Thus, the Raf-1/MEK1/2/ERK1/2 and JNK1/2 pathways were significantly upregulated in response to increases of GM1 in co-cultured xenogeneic cells. However, the inflammatory response was suppressed in co-culture of GM1-knockdown pADMSCs with RAW264.7 cells via down-regulation of the Raf-1/MEK1/2/ERK1/2 and JNK1/2 pathways. Therefore, the ganglioside GM1 appears to play a major role in the inflammatory response in xenotransplantation via the Raf-1/MEK1/2/ERK1/2 and JNK1/2 pathways. 

Retracted: No

PubPeer comments:
 Figure 1B: * Red boxes: The same band - with a little dot on the left - appears to be visible four times * Yellow boxes: The same band appears to be visible twice Could the authors please take away any concern by showing the original uncroppped gel? ![file] ,
Cyclometalated [Cp*M(C^X)] (M = Ir, Rh; X = N, C, O, P) complexes
Authors: Ying-Feng Han
Guo-Xin Jin
Journal: Chemical Society Reviews (2014)
Discipline: CHEMISTRY
Keywords: Half-sandwich; Cp*Ir; Cp*Rh; metalacycles; organic transformations
Affiliations: Shanghai Key Laboratory of Molecular Catalysis and Innovative Material

Abstract:  Half-sandwich Cp*Ir and Cp*Rh metalacycles have been successfully applied in traditional domains encompassing organic transformations and catalysis in recent years, especially the catalytic activation of C-H bonds. Cyclometalation has proven to be a highly attractive and versatile synthetic method for the formation of organometallic metalacycles. This review intends to describe isolated and well-defined cyclometalated iridium/rhodium complexes that contain a Cp*M-C (M = Ir, Rh) bond stabilised by the intramolecular coordination of neutral donor atoms (N, C, O or P). The formation of metalamacrocycles and cages employing cyclometalated approaches is discussed. In focusing on selected mechanistic insights garnered from iridium/rhodium-catalysed functionalisation of C-H bonds involving cyclometalated complexes, a limited number of substrates will be discussed, but a broad range of mechanistic features is highlighted. 

Retracted: No

PubPeer comments:
 There are many splice sites (indicated with red arrow) in Fig 2B. ![file] ,