PReD-Bench/PRed-Bench huggingface dataset:
Long non-coding RNA HOXA11-AS accelerates the progression of keloid formation via miR-124-3p/TGFβR1 axis
Authors: Xiao-Hua Luo
Hong-Feng Zhai
Jun Jin
Zhen-Hua Jia
Journal: Cell Cycle (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Keloid formation; TGFβ receptor type I; lncRNA HOXA11-AS; miR-124-3p.
Affiliations: Department of Plastic Surgery, People’s Hospital of Zhengzhou University, Henan People’s Hospital, Zhengzhou, P.R. China

Abstract:  Emerging evidence reveals the importance of long non-coding RNAs (lncRNAs) in the development and progression of keloid formation, whereas the underlying mechanisms are not well understood. In the present study, we investigated the biological effects and molecular mechanisms of lncRNA HOXA11-AS in keloid formation. First, the expression levels of HOXA11-AS, miR-124-3p, and transforming growth factor β receptor type I (TGFβR1) were measured in both keloid tissues and human keloid fibroblasts (HKFs) using qRT-PCR and western blot analysis, respectively. Next, we adopted both gain- and loss-of-function strategies to explore the significance of HOXA11-AS. TUNEL, flow cytometry, DNA ladder, and tube formation assays were performed to measure cell apoptosis and angiogenesis, respectively. Besides, the potential binding relationship between HOXA11-AS and miR-124-3p, as well as miR-124-3p and TGFβR1 was identified using bioinformatic screening and verified by luciferase reporter assay. Furthermore, we explored the importance of miR-124-3p in HOXA11-AS-induced phenotypes and regulations on TGFβ signaling or PI3K/Akt signaling. We found that HOXA11-AS and TGFβR1 were significantly up-regulated, while miR-124-3p was down-regulated both in keloid tissues or fibroblasts than in normal skin tissues or fibroblasts. Functionally, high expression of HOXA11-AS essentially inhibited cell apoptosis and promoted fibroblast-induced angiogenesis. Mechanistically, miR-124-3p was identified as a downstream effector to be involved in HOXA11-AS-mediated phenotypes through directly targeting TGFβR1, thus modulating PI3K/Akt signaling pathway. Taken together, our findings revealed that HOXA11-AS inhibits cell apoptosis and promotes angiogenesis through miR-124-3p/TGFβR1 axis, contributing to the progression of keloid formation, which might provide a novel target for keloid therapy. 

Retracted: No

PubPeer comments:
 In Figure 4b, a micrograph has been duplicated and presented as something else. ![file] ,
<p>Curcumin Inhibits the Tumorigenesis of Breast Cancer by Blocking Tafazzin/Yes-Associated Protein Axis</p>
Authors: Shuang Liu
Yuxiu Shen
Ying Li
Yang Jiao
Hongyan Yuan
Zaigang Han
Journal: Cancer Management and Research (2020)
Discipline: CLINICAL MEDICINE
Keywords: Hippo signaling pathway; breast cancer; curcumin; metastasis; proliferation.
Affiliations: Department of Pharmacology, Affiliated Hospital of Beihua University, Jilin City, Jilin Province 132000, People's Republic of China.

Abstract:  Purpose: This study was aimed to explore the anti-tumor effect of curcumin on breast cancer (BC) and the underlying mechanism involving Tafazzin (TAZ)/Yes-associated protein (YAP) axis. Methods: Different concentrations of curcumin (0, 10, 20 and 30 μM) were used to treat BC cells (MCF-7 and MDA-MB-231 cells). The viability, colony formation, apoptosis, migration, and invasion of BC cells were detected by MTT, colony formation, flow cytometry, wound-healing and transwell assay, respectively. The protein expression of TAZ and YAP (effectors of Hippo signaling pathway) was detected by Western blot. MDA-MB-231 cells were injected into mice to verify the anti-tumor effect of curcumin in vivo. Results: Curcumin (20 and 30 μM) inhibited the proliferation, migration and invasion, and promoted the apoptosis of MCF-7 and MDA-MB-231 cells. Curcumin decreased the protein expression of TAZ and YAP in MCF-7 and MDA-MB-231 cells. Overexpression of YAP reversed the anti-tumor effect of curcumin on MDA-MB-231 cells. In addition, curcumin (100, 200 and 300 mg/kg/d) inhibited the growth of tumor xenografts in mice, and down-regulated the protein expression of TAZ and YAP in tumor xenografts. However, curcumin at a concentration of 300 mg/kg/d slowed the increasing of body weight in mice. Conclusion: Curcumin inhibited the tumorigenesis of BC by blocking TAZ/YAP axis. 

Retracted: Yes

PubPeer comments:
 Figure 2A has some issues. There appear to be repeated patterns (or motifs) in multiple images. My notations attempt to illustrate some of these, but are not exhaustive. Other readers may wish to be more thorough. The cyan boxes indicate the location of the two close-ups below. *** ![file] *** Closeup 1 with Forensically illustration ![file] *** Closeup 2 ![file] , 
 #1 ![file] , 
 Fig 1B, let me introduce you to Fig 4B. But maybe you already know each other. ![file] , 
 #1 Fig 4D follows a simple pattern: the 0-hour and 48-hour images are the same, but with a vertical flip and narrower central gray bands in the 48-hour versions. ![file] , 
 July 14, 2020 The Editor and Publisher of Cancer Management and Research wish to retract the published article. We were notified of potential image manipulation in the published article. The issues relate to the alleged duplication of images shown in Figures 1B, which appear to be duplicated with images shown in Figure 4B. Our other in Figures 2A, 4D and 5A. Despite repeated attempts to contact the authors, they have not responded to our queries within the required timeframe. The editor determined the findings of the study were no longer valid and requested for the article to be retracted. ,
Adipose is a conserved dosage-sensitive antiobesity gene
Authors: Renee McKay
Jae Myoung Suh
Jin Seo
Michael Wang
Jonathan M Graff
Zack Salo
Robert Li
Daniel Zeve
Journal: Cell Metabolism (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Adipose; anti-obesity function; fat formation; dosage-sensitive; obesity
Affiliations: Department of Developmental Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, NB5.118, Dallas, TX 75390-9133, USA.

Abstract:  Adipose (Adp) is an evolutionarily conserved gene isolated from naturally occurring obese flies homozygous for an adp mutation. Here we show that the anti-obesity function of Adp (worm Y73E7A.9, fly adp, and murine Wdtc1) is conserved from worms to mammals. Further, Adp appears to inhibit fat formation in a dosage-sensitive manner. Adp heterozygous flies and Adp heterozygous mutant mice are obese and insulin resistant, as are mice that express a dominant negative form of Adp in fat cells. Conversely, fat-restricted Adp transgenic mice are lean and display improved metabolic profiles. A transient transgenic increase in Adp activity in adult fly fat tissues reduces fat accumulation, indicating therapeutic potential. ADP may elicit these anti-adipogenic functions by regulating chromatin dynamics and gene transcription, as it binds both histones and HDAC3 and inhibits PPARgamma activity. Thus Adp appears to be involved in an ancient pathway that regulates fat accumulation. 

Retracted: No

PubPeer comments:
 Fig. 5E: More similar than expected, could authors please check? ![file] , 
 The region of similarity actually extends further - the bottom quarter of the  ING WAT figure is the same as the top of the  GON WAT figure. ![file] ,
Soy protein preserves basement membrane integrity through a synergistic effect on nephrin, matrix metalloproteinase and vascular endothelial growth factor
Authors: Carani Venkataraman Anuradha
Nallasamy Palanisamy
Journal: American Journal of Nephrology (2011)
Discipline: CLINICAL MEDICINE
Keywords: Soy protein; Renal function; Albuminuria; Basement membrane integrity; Insulin sensitivity
Affiliations: Department of Biochemistry and Biotechnology, Annamalai University, India. 

Abstract:  Background/aims: Soy protein improves renal function and prevents albuminuria in diabetic rats. This study investigates whether the renoprotective effect of soy protein is related to sustenance of basement membrane integrity. Methods: Adult male albino rats were randomized into four groups and fed one of the following semi-synthetic diets consisting of corn starch (60%) and casein (20%; CCD), fructose (60%) and casein (20%; FCD), fructose (60%) and soy protein (20%; FSD), or corn starch (60%) and soy protein (20%; CSD). Plasma chemistry and renal changes were analyzed after 60 days. Results: FCD rats displayed metabolic derangements and renal ultrastructural changes. FSD rats showed reduction in type IV collagen, tissue inhibitor for matrix metallo-proteinase-2, vascular endothelial growth factor and tumor necrosis factor-α expression and improved matrix metallo-proteinase expression. Renal architecture was preserved in these rats. Conclusion: Soy protein supplementation not only improved insulin sensitivity but also markedly attenuated renal basement membrane changes in fructose diet-fed rats. These findings provide evidence in support of the use of dietary soy protein in patients with diabetic kidney disease. 

Retracted: No

PubPeer comments:
 This paper largely overlaps with [Arshad et al 2016] . Some text also overlaps [Kapratwar 2016] , a master s thesis. In the attached image, Arshad et al 2016 is on the left, Patil and Patil 2018 is on the right. ![file] , 
 In looking at this a bit further, the paper also has exact text from [Mohini et al 2013](http: www.isca.in COM_IT_SCI Archive v1 i6 3.ISCA-RJCITS-2013-030.php), [Ramachandran et al 2012] , and two of the first author s other papers,[ Patil and Jadav 2017](http: www.ijlret.com Papers Vol-3-issue-3 12-B2017066.pdf), and [Patil and Joshi 2014] . There are just a few sentences in the paper that I haven t found in other work. ,
Effects of curcumin on the role of MMP-2 in endometrial cancer cell proliferation and invasion
Authors: G-L Fan
F Yu
M-X Sun
M-L Gong
C-X Liu
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Curcumin concentrations; proliferation; invasion; endometrial cancer cells; MMP-2
Affiliations: Department of Obstetrics and Gynecology, Beijing Chaoyang Hospital West, Beijing P.R. China. .

Abstract:  Objective: This study aims to investigate the effect of curcumin concentrations on the proliferation and invasion of endometrial cancer cells. Materials and methods: Endometrial cancer cells were cultured with 0, 15, and 30 μmol/l curcumin, and were divided into control group, low concentration group, and high concentration group. The treatment included the silencing and overexpression of MMP-2. The expression of MMP-2 and E-cadherin were detected by Western blot and the expression level changes were recorded after MMP-2 was silenced and overexpressed. Pearson's analysis was used to determine the relationship of curcumin concentration between MMP-2 mRNA. CCK-8 was used to detect the optical density of cancer cells in three groups. Transwell invasion assay was performed to analyze the invasion inhibition rate in the three groups. Results: Western blot and qPCR results: MMP-2 expression levels were lower and E-cadherin was higher in high concentration group than that in the low concentration group (p&lt;0.01). MMP-2 protein and mRNA decreased after ShRNA and increased after overexpression (p&lt;0.01). Pearson analysis revealed that the curcumin concentration was negatively correlated with the MMP-2 mRNA (r=-0.497, p=0.036). Cell optical density was lower with curcumin and the lowest was in high concentration group (p&lt;0.01). After MMP-2 silencing, optical cell density decreased and this value increased after overexpression (p=0.000). Cell invasion results: Curcumin improves the rate of cell invasion (p&lt;0.01). After silencing of MMP-2, cell invasion inhibition rate increased, while the invasion inhibition rate decreased after overexpression (p&lt;0.01). Conclusions: Curcumin can downregulate MMP-2, inhibit the proliferation and invasion of cancer cells. 

Retracted: No

PubPeer comments:
 Figure 1 and Figure 4: * Red boxes: The b-actin panel appears to be identical in both figures, even though the lanes represent different samples. ![file] ,
Microstructural and Nanostructural Evolution of Light Harvester Perovskite Thin Film under the Influence of Ultrasonic Vibrations
Authors: Claire Barratt
Amin Rahimzadeh
Morteza Eslamian
Mohammad-Reza Ahmadian-Yazdi
Journal: ACS Omega (2020)
Discipline: CHEMISTRY
Keywords: perovskite thin-film; post-treatment process; ultrasonic vibrations; solvent evaporation; nucleation
Affiliations: University of Michigan-Shanghai Jiao Tong University, Shanghai 200240, China

Abstract:  A key step of inexpensive and scalable perovskite thin-film formation is defect-free fabrication through low-cost and facile post-treatment processes. Methods using high annealing temperatures are not favorable for the scale-up of solution-processed thin-film solar cells, particularly on plastic/flexible substrates. This contribution analyzes the effect of ultrasonic vibrations, a recently developed low-cost post-treatment process, on thin-film quality. Ultrasonic vibrations were applied to as-spun CH3NH3PbI3 perovskite thin films prepared with various solvents and antisolvents deposited on substrates with compact and mesoporous textures. Then, mechanisms of solvent evaporation, nucleation, and crystallization of perovskite grains were characterized during ultrasonic vibration. These studies demonstrate that ultrasonic vibration at low temperature facilitates heterogeneous crystallization of perovskite grains with a higher conversion of nuclei into crystal, compared with the conventional annealing process. Topographic scanning electron microscopy images confirm the dense and fully covered thin films after the evaporation of solvent. Furthermore, it is shown that crystal orientation does not change with the choice of solvent, eliminating the effect of solvent on the deposition of thin-film perovskites with this method. Therefore, this ultrasonic vibration post-treatment method is applicable to any solution-processed material and deposition technique, and it can be used to fabricate a range of thin-film devices and printed electronics. 

Retracted: No

PubPeer comments:
 Figure 12B: * Blue box: In the third panel from the top, both plots appear to look identical. ![file] ,
Amyloid Form of Ovalbumin Evokes Native Antigen-specific Immune Response in the Host
Authors: Renu Balyan
Mohammad Owais
Swaleha Zubair
Manzoor Ahmad Gatoo
Mohd Asif Sherwani
Mohd Saad Umar
Syed Mohd Faisal
Jasneet Kaur Khalsa
Shadab Kazmi
Saba Tufail
Journal: Journal of Biological Chemistry (2015)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Albumin; Amyloid; Antibody; Antigen; Antigen Presentation.

Abstract:  Amyloids are highly organized protein aggregates that arise from inappropriately folded versions of proteins or polypeptides under both physiological as well as simulated ambiences. Once thought to be irreversible assemblies, amyloids have begun to expose their more dynamic and reversible attributes depending upon the intrinsic properties of the precursor protein/peptide and experimental conditions such as temperature, pressure, structural modifications in proteins, or presence of chemicals in the reaction mixture. It has been repeatedly proposed that amyloids undergo transformation to the bioactive peptide/protein forms under specific conditions. In the present study, amyloids assembled from the model protein ovalbumin (OVA) were found to release the precursor protein in a slow and steady manner over an extended time period. Interestingly, the released OVA from amyloid depot was found to exhibit biophysical characteristics of native protein and reacted with native-OVA specific monoclonal as well as polyclonal antibodies. Moreover, antibodies generated upon immunization of OVA amyloidal aggregates or fibrils were found to recognize the native form of OVA. The study suggests that amyloids may act as depots for the native form of the protein and therefore can be exploited as vaccine candidates, where slow antigen release over extended time periods is a pre-requisite for the development of desired immune response. 

Retracted: No

PubPeer comments:
 Figure 5D-c * Red boxes: In the Native OVA column the panels representing pH 2.5 and 7.0 appear to showing the same sample. ![file] ,
Exercise Training in Obese Rats Does Not Induce Browning at Thermoneutrality and Induces a Muscle-Like Signature in Brown Adipose Tissue
Authors: Helen Budge
Michael E Symonds
Peter Aldiss
Francis J P Ebling
David J Boocock
Ian Bloor
Jo E Lewis
Irene Lupini
Amanda K Miles
Ramyar Chavoshinejad
Journal: Frontiers in endocrinology (2020)
Discipline: CLINICAL MEDICINE
Keywords: adipose tissue; browning; exercise training; housing temperature; obesity.
Affiliations: The Early Life Research Unit, Division of Child Health, Obstetrics and Gynaecology, School of Medicine, University of Nottingham, Nottingham, United Kingdom., School of Life Sciences, Queen's Medical Centre, University of Nottingham, Nottingham, United Kingdom., School of Biosciences and Veterinary Medicine, University of Camerino, Camerino, Italy., John van Geest Cancer Research Centre, Nottingham Trent University, Nottingham, United Kingdom., Nottingham Digestive Disease Centre and Biomedical Research Unit, School of Medicine, University of Nottingham, Nottingham, United Kingdom.

Abstract:  Aim: Exercise training elicits diverse effects on brown (BAT) and white adipose tissue (WAT) physiology in rodents housed below their thermoneutral zone (i.e., 28-32°C). In these conditions, BAT is chronically hyperactive and, unlike human residence, closer to thermoneutrality. Therefore, we set out to determine the effects of exercise training in obese animals at 28°C (i.e., thermoneutrality) on BAT and WAT in its basal (i.e., inactive) state. Methods: Sprague-Dawley rats (n = 12) were housed at thermoneutrality from 3 weeks of age and fed a high-fat diet. At 12 weeks of age half these animals were randomized to 4-weeks of swim-training (1 h/day, 5 days per week). Following a metabolic assessment interscapular and perivascular BAT and inguinal (I)WAT were taken for analysis of thermogenic genes and the proteome. Results: Exercise attenuated weight gain but did not affect total fat mass or thermogenic gene expression. Proteomics revealed an impact of exercise training on 2-oxoglutarate metabolic process, mitochondrial respiratory chain complex IV, carbon metabolism, and oxidative phosphorylation. This was accompanied by an upregulation of multiple proteins involved in skeletal muscle physiology in BAT and an upregulation of muscle specific markers (i.e., Myod1, CkM, Mb, and MyoG). UCP1 mRNA was undetectable in IWAT with proteomics highlighting changes to DNA binding, the positive regulation of apoptosis, HIF-1 signaling and cytokine-cytokine receptor interaction. Conclusion: Exercise training reduced weight gain in obese animals at thermoneutrality and is accompanied by an oxidative signature in BAT which is accompanied by a muscle-like signature rather than induction of thermogenic genes. This may represent a new, UCP1-independent pathway through which BAT physiology is regulated by exercise training. 

Retracted: No

PubPeer comments:
 ![file] , 
 #1 Hi, thanks for spotting this. These are representative images from either C or Ex groups, seems I selected the same one twice and didn t realise, or catch at proof stage. Will get this sorted asap. Thanks again, Pete ,
Transcriptome profiling analysis reveals that CXCL2 is involved in anlotinib resistance in human lung cancer cells
Authors: Shuyuan Wang
Jie Qian
Bo Zhang
Jun Lu
Lele Zhang
Wei Xu
Minjuan Hu
Xiaodong Zhao
Rong Qiao
Baohui Han
Yiming Zhao
Journal: BMC Medical Genomics (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Anlotinib; CXCL2; Drug resistance; Non-Small Cell Lung Cancer; Transcriptome.
Affiliations: Department of Pulmonary Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, 241 Huaihai West Rd, Shanghai, 200030, China., Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, 800 Dong Chuan Rd, Shanghai, 200240, China., Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, 800 Dong Chuan Rd, Shanghai, 200240, China. ., Department of Pulmonary Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, 241 Huaihai West Rd, Shanghai, 200030, China. .

Abstract:  Background: Anlotinib has been demonstrated its anti-tumor efficacy on non-small cell lung cancer (NSCLC) in clinical trials at 3rd line. However, anlotinib resistance occurs during its administration, and the underlying mechanism is still unclear. Methods: Anlotinib resistant lung cancer cell line NCI-H1975 was established in vitro. Toxicologic effects undergoing anlotinib stress were observed upon NCI-H1975 cells and anlotinib resistant NCI-H1975 cells, respectively. Transcriptome profiling was performed to screen anlotinib resistance-associated genes between NCI-H1975 cells and anlotinib resistant NCI-H1975 cells. Functional assays were performed to examine the correlations between CXCL2 gene expression and anlotinib resistance. Results: We found anlotinib inhibits cell proliferation and cell viability in NCI-1975 cells, whereas it attenuates these activities in anlotinib resistant NCI-H1975 cells. Transcriptome profiling analysis identified 769 anlotinib-responsive genes enriched in the biological processes of microtubule-based process, cytoskeleton organization, and wound healing. Furthermore, we found 127 genes are associated with anlotinib resistance. In particular, we demonstrated that CXCL2 contributes to anlotinib resistance in NCI-H1975 cells. Conclusions: This study suggested that CXCL2 is involved in anlotinib resistance in NCI-H1975 cells and provided an insight for understanding the resistant mechanism of anlotinib. 

Retracted: No

PubPeer comments:
 Two images in Figure 4A appear to overlap, but are described differently. *** ![file] *** Funding Publication of this article was supported by the program of system biomedicine innovation center from Shanghai Jiao Tong University (Project No. 15ZH4009); the key program of translational medicine from Shanghai Jiao Tong University School of Medicine (Project No. 15ZH1008); National Natural Science Foundation of China (Project No. 81673015); and the project of Science and Technology Commission of Shanghai Municipality (Project No. 16140902700). ,
IRE1α-XBP1s pathway promotes prostate cancer by activating c-MYC signaling
Authors: Lukas Simon
Su Qu
Hatice Zeynep Nenseth
Qingping Zeng
Håvard Danielsen
Stephanie Greene
Turid Frahnow
Yang Jin
John B Patterson
Fahri Saatcioglu
Xia Sheng
Fabian Theis
Ladan Fazli
Omer F Kuzu
Ian G Mills
Paul S Rennie
Journal: Nature Communications (2019)
Discipline: Multidisciplinary
Keywords: Endoplasmic reticulum stress; Unfolded protein response; Cancer; IRE1α; MKC8866
Affiliations: Department of Biosciences, University of Oslo, 0316, Oslo, Norway., School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 430030, Wuhan, China., Institute of Computational Biology, Helmholtz Zentrum München, 85764, Neuherberg, Germany., Faculty of Business Administration and Economics, Chair DataScience, University Bielefeld, 33615, Bielefeld, Germany., Fosun Orinove, Inc., Unit 211, Building A4, 218 Xinhu Street, 215000, SuZhou, China., The Vancouver Prostate Centre, Vancouver, BC, V6H3Z6, Canada., Movember/PCUK Centre of Excellence for Prostate Cancer Research, Centre for Cancer Research and Cell Biology (CCRCB), Queen's University of Belfast, Belfast, BT7 1NN, UK., Institute for Cancer Genetics and Informatics, Oslo University Hospital, 0379, Oslo, Norway., Center for Cancer Biomedicine, University of Oslo, 0316, Oslo, Norway., Department of Informatics, University of Oslo, 0316, Oslo, Norway., Nuffield Division of Clinical Laboratory Sciences, University of Oxford, Oxford, OX3 7LF, UK., Department of Biosciences, University of Oslo, 0316, Oslo, Norway. ., Institute for Cancer Genetics and Informatics, Oslo University Hospital, 0379, Oslo, Norway. .

Abstract:  Activation of endoplasmic reticulum (ER) stress/the unfolded protein response (UPR) has been linked to cancer, but the molecular mechanisms are poorly understood and there is a paucity of reagents to translate this for cancer therapy. Here, we report that an IRE1α RNase-specific inhibitor, MKC8866, strongly inhibits prostate cancer (PCa) tumor growth as monotherapy in multiple preclinical models in mice and shows synergistic antitumor effects with current PCa drugs. Interestingly, global transcriptomic analysis reveal that IRE1α-XBP1s pathway activity is required for c-MYC signaling, one of the most highly activated oncogenic pathways in PCa. XBP1s is necessary for optimal c-MYC mRNA and protein expression, establishing, for the first time, a direct link between UPR and oncogene activation. In addition, an XBP1-specific gene expression signature is strongly associated with PCa prognosis. Our data establish IRE1α-XBP1s signaling as a central pathway in PCa and indicate that its targeting may offer novel treatment strategies. 

Retracted: No

PubPeer comments:
 In Figure 4h, an image has been duplicated, modified and presented as something else. The raw data for the Western immunoblotting data shown in the supplementary, seem to be retrieved from different experiments gel run. e.g. Figure 1b: the presented membranes show variation in number of lanes and + - MW lane. Figure 4e: some of the membranes have different size. ![file] ![file] ![file] ,
Hypoxia-Induced WSB1 Promotes the Metastatic Potential of Osteosarcoma Cells
Authors: Ji Cao
Bo Yang
Ning Zhang
Rong Dong
Yijie Wang
Jing Wang
Meidan Ying
Qiaojun He
Guanyu Lin
Nengming Lin
Ling Ding
Yongchuan Gu
Journal: Cancer Research (2015)
Discipline: CLINICAL MEDICINE
Keywords: Intratumoral hypoxia; solid tumors; metastatic character; E3 ubiquitin ligase; WSB1
Affiliations: Institute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China., Department of Orthopedics, The Second Affiliated Hospital of Zhejiang University, Zhejiang University, Hangzhou, China., Zhejiang Province Key Laboratory of Medical Molecular Imaging, The Second Affiliated Hospital of Zhejiang University, Zhejiang University, Hangzhou, China., Institute for Individualized Medicine, Hangzhou First People's Hospital, Hangzhou, China., Auckland Cancer Society Research Centre, The University of Auckland, Auckland, New Zealand., Institute of Pharmacology and Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China. .

Abstract:  Intratumoral hypoxia occurs in many solid tumors, where it is associated with the development of metastatic character. However, the connections between these phenomena are not fully understood. In this study, we define an integrative role for the E3 ubiquitin ligase subunit WSB1. In primary osteosarcomas, increased levels of WSB1 correlated with pulmonary metastatic potential. RNAi-mediated attenuation of WSB1 or disruption of its E3 ligase activity potently suppressed tumor metastasis. Quantitative proteomic and functional analyses revealed that WSB1 ubiquitylates the Rho-binding protein RhoGDI2 and promotes its proteasomal degradation, thereby activating Rac1 to stimulate tumor cell motility and invasion. Our findings show how WSB1 regulates key steps of the metastatic cascade in hypoxia-driven osteosarcoma, and they highlight a candidate therapeutic target to potentially improve the survival of patients with metastatic disease. 

Retracted: No

PubPeer comments:
 Clockwise from upper left: - Fig 3A,B from  p63 protects chondrosarcoma malignancies mainly by enhancing the expression of PTEN [(Ding et al 2017)] . - Fig 3B from  Antisense lncRNA As-SLC7A11 suppresses epithelial ovarian cancer progression mainly by targeting SLC7A11 [(Yuan, Liu Song 2017)] . - Fig 3A,B from  MiR-139 prompts the development of osteosarcomas mainly through targeting ROCK1 [(Su Nie 2017)] . - Fig 2B from  Reduced lncRNA Aim enhances the malignant invasion of triple-negative breast cancer cells mainly by activating Wnt u03b2-catenin mTOR PI3K signaling **[(Liu et al 2017)] **. ![] The publishers should consider the possibility that the editorial or peer-review processes of  Die Pharmazie have been subverted. ,
METTL1 Promotes let-7 MicroRNA Processing via m7G Methylation
Authors: Byron Andrews
Natalie Webster
Valentina Migliori
Pierre Murat
Shankar Balasubramanian
Alan Hendrick
Samuel C Robson
Luca Pandolfini
Andrej Alendar
Isaia Barbieri
Mara d&#x27;Onofrio
Rossella Brandi
Andrew J Bannister
Tony Kouzarides
Pia Mach
Journal: Molecular Cell (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: 7-methylguanosine; G-quadruplexes; METTL1; RNA methylation; SAM-dependent methyltransferase
Affiliations: The Gurdon Institute and Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK., The Gurdon Institute and Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK; Division of Cellular and Molecular Pathology, Department of Pathology, University of Cambridge, Addenbroke's Hospital, Cambridge CB2 0QQ, UK., Storm Therapeutics, Ltd., Moneta Building (B280), Babraham Research Campus, Cambridge CB22 3AT, UK., Department of Chemistry, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, UK., Fondazione EBRI Rita Levi-Montalcini, Genomics Laboratory, Viale Regina Elena 295, 00161 Rome, Italy., Fondazione EBRI Rita Levi-Montalcini, Genomics Laboratory, Viale Regina Elena 295, 00161 Rome, Italy; IFT-CNR, Via del Fosso del Cavaliere 100, 00133 Rome, Italy., The Gurdon Institute and Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK. Electronic address: .

Abstract:  7-methylguanosine (m7G) is present at mRNA caps and at defined internal positions within tRNAs and rRNAs. However, its detection within low-abundance mRNAs and microRNAs (miRNAs) has been hampered by a lack of sensitive detection strategies. Here, we adapt a chemical reactivity assay to detect internal m7G in miRNAs. Using this technique (Borohydride Reduction sequencing [BoRed-seq]) alongside RNA immunoprecipitation, we identify m7G within a subset of miRNAs that inhibit cell migration. We show that the METTL1 methyltransferase mediates m7G methylation within miRNAs and that this enzyme regulates cell migration via its catalytic activity. Using refined mass spectrometry methods, we map m7G to a single guanosine within the let-7e-5p miRNA. We show that METTL1-mediated methylation augments let-7 miRNA processing by disrupting an inhibitory secondary structure within the primary miRNA transcript (pri-miRNA). These results identify METTL1-dependent N7-methylation of guanosine as a new RNA modification pathway that regulates miRNA structure, biogenesis, and cell migration. 

Retracted: No

PubPeer comments:
 The paper below refutes the findings of the above paper https: www.sciencedirect.com science article pii S1097276520303427 and the authors response is here https: www.sciencedirect.com science article pii S1097276520303439 ,
Correlations between claudin-1 and PIGF expressions in retinoblastoma
Authors: Z-Y Zhou
H-F Wang
S-F Zheng
J Xu
Y Chen
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: claudin-1; PlGF; retinoblastoma; differentiation; infiltration
Affiliations: Department of Ophthalmology, People's Hospital of Weifang, Weifang, Shandong, China. .

Abstract:  Objective: To investigate the expressions of claudin-1 and placental growth factor (PlGF) proteins in retinoblastoma (RB) and their relationships with the differentiation of RB, the infiltration of optic nerve and choroid and clinical stages. Patients and methods: Immunohistochemical (IHC) method was used to detect the expressions of claudin-1 and PlGF proteins in 56 cases of RB paraffin-embedded tissue samples. The x2-test and Fisher exact test were used to compare the qualitative variables. The Pearson correlation coefficient was used to detect the correlation of the expression of claudin-1 with that of PlGF in RB tissues. Results: 1) Among RB tissues, the positive expression rates of claudin-1 in clinical stage I tumors and clinical stage III tumors were 69.2% and 38.9%, respectively, and claudin-1 was not expressed in all clinical stage II tumors (p=0.002). In case of optic nerve invasion, the lowly positive expression of claudin-1 was detected, and the difference was significant (p=0.001). 2) The positive expression rate of PlGF proteins in RB was 73.8%, which was higher in tumors with optic nerve invasion than in tumors without the invasion; the expression was significantly different (p=0.001). In addition, the positive expression rate of PlGF in tumors with choroidal invasion was 74.1%. 3) The expression of claudin-1 in RB was negatively correlated with the presence of choroidal invasion (r=0.52, p≤0.0001) and optic nerve infiltration (r=0.49, p=0.0003). There was a significant positive correlation between the expression of PlGF and the presence of optic nerve invasion (r=0.30, p=0.009). In addition, there was a significant positive correlation between the expression of claudin-1 and that of PlGF (r=0.41, p=0.006). Conclusions: The expression level of claudin-1 is negatively correlated with the differentiation of RB cells, optic nerve infiltration and clinical stages, while the expression of PlGF was positively correlated with the optic nerve infiltration and clinical stages of RB. The role of claudin-1 may be opposite to that of matrix metalloproteinase-2 (MMP-2) in the development of RB. 

Retracted: No

PubPeer comments:
  All patients who participated in the study **signed the written informed consent** prior to surgery . Average age of the infants and young children in this study was 22 months ( range: 3-48 months ). The 3-month-old infant s writing skills were especially precocious. ,
RETRACTED ARTICLE: microRNA-128 mediates CB1 expression and regulates NF-KB/p-JNK axis to influence the occurrence of diabetic bladder disease
Authors: Kewei Fang
Xin Gou
Jing Wu
Yuting Weng
Guiqing Li
Tao Chen
Tongxin Yang
Mingqing Huang
Journal: Journal of Translational Medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: Apoptosis; Bladder disease; CB1; Diabetes; NF-KB
Affiliations: Department of Urology, The Second Affiliated Hospital of Kunming Medical University, No. 374, Dianmian Dadao, Kunming, Yunnan, 650101, People's Republic of China., Department of Biochemistry and Molecular Biology, The Primary Medicine School of Kunming Medical University, Kunming, 650101, People's Republic of China., Department of Urology, The 2nd Hospital of Kunming Medical University, Kunming, 650101, People's Republic of China., Department of Urology, The Second Affiliated Hospital of Kunming Medical University, No. 374, Dianmian Dadao, Kunming, Yunnan, 650101, People's Republic of China. .

Abstract:  Background: Diabetic bladder disease is common complications of diabetes, its symptoms are diverse, can be due to different stages. In this study we investigate the mechanism of miR-128 targeting CB1 expression to mediate the occurrence of diabetic bladder disease. Methods: Bioinformatics analysis predicts related regulatory factors of miR-128 in diabetic bladder disease. Models of diabetic bladder lesions were constructed in male SD rats by intraperitoneal injection of streptozotocin at 65 mg/kg body weight. The expression of miR-128 and CB1 mRNA in bladder tissues of each group was detected by RT-qPCR, and CB1, NF-KB, p-JNK and Bcl2 protein expression was detected by Western Blotting. We tested the function of the bladder by urodynamics, detected the pathological characteristics of the bladder tissue by HE staining, and verified the targeting relationship between miR-128 and CB1 through the prediction of the biological website, dual luciferase reporter gene assay and RIP. Results: miR-128 was highly expressed in the bladder tissue of diabetic rats. Inhibition of miR-128 could improve the occurrence of diabetic bladder lesions in rats. miR-128 could target the inhibition of CB1 expression, and high expression of CB1 could antagonize miR-128 against diabetic bladder. In the diabetic bladder, miR-128 can regulate the expression of NF-KB and p-JNK through CB1 and affect the level of apoptosis. miR-128 regulates NF-KB/p-JNK through CB1, thus affecting the occurrence of diabetic bladder disease. Conclusion: The high expression of miR-128 can down-regulate the expression of CB1, promote the activation of NF-KB and p-JNK, increase the level of apoptosis and promote the occurrence of diabetic bladder disease. 

Retracted: Yes

PubPeer comments:
 Figure 5. Much more similar than you would expect. https: imgur.com 4O0s0K3 ,
Structure-induced enhancement in electrooxidation of trimetallic FePtAu nanoparticles
Authors: Shaojun Guo
Dong Su
Shouheng Sun
Sen Zhang
Huiyuan Zhu
Journal: Journal of the American Chemical Society (2012)
Discipline: CHEMISTRY
Keywords: FePtAu nanoparticles; structure-control strategy; NP catalysis; Au; FePt structure transformation
Affiliations: Department of Chemistry, Brown University, Providence, Rhode Island 02912, United
States, Center for Functional
Nanomaterials, Brookhaven National Laboratory, Upton, New York 11973,
United States

Abstract:  Using FePtAu nanoparticles (NPs) as an example, this Communication demonstrates a new structure-control strategy to tune and optimize NP catalysis. The presence of Au in FePtAu facilitates FePt structure transformation from chemically disordered face-centered cubic (fcc) structure to chemically ordered face-centered tetragonal (fct) structure, and further promotes formic acid oxidation reaction (FAOR). The fct-FePtAu NPs have mass activity as high as 2809.9 mA/mg Pt and retain 92.5% of this activity after a 13 h stability test. They become the most efficient NP catalyst ever reported for FAOR. This structure-control strategy can be extended to other multimetallic NP systems, providing a general approach to advanced NP catalysts with desired activity and durability control for practical applications. 

Retracted: No

PubPeer comments:
 Could the authors explain the reasoning behind the choice of References [8,9]?  To date, much efforts have been devoted to the design and preparation of transition metal coordination polymer materials because these metals are physiologically essential metal elements that function in endogenous oxidative DNA damage associated with aging and cancer.[4u20138] - [8]. Liu, W.; Li, H.; Zhu, H.; Xu, P. **The Interfacial Adhesion Performance and Mechanism of a Modified Asphaltu2013Steel Slag Aggregate**. Materials 2020, 13, 1180. DOI: 10.3390 ma13051180.  Besides, coordination polymers can interact with DNA through noncovalent interactions, including intercalation and groove binding for large molecules and slot external electrostatic binding for cations.[9u201314] - [9]. Wang, Z.; Zhang, X.; Jiang, S.; Qu, Y.; Ou, D.; Wang, J. **Arc Erosion Dynamic of Island-and Skeleton-Restricted Microstructure Evolution Modes in Agu2013CuO Contact Materials**. J. Alloy. Compd. 2020, 828, 154412. DOI: 10.1016 j.jallcom.2020.154412. , 
 Is this a misspelling of [u201clogarithmic growth phaseu201d] ? ![file] Found with the [_Problematic Paper Screener_] . ,
AURKA contributes to the progression of oral squamous cell carcinoma (OSCC) through modulating epithelial-to-mesenchymal transition (EMT) and apoptosis via the regulation of ROS
Authors: Hou Dawei
Dong Honggang
Wang Qian
Journal: Biochemical and Biophysical Research Communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: AURKA; Apoptosis; EMT; ROS generation; oral squamous cell carcinoma (OSCC).
Affiliations: Department of Oral and Maxillofacial Surgery, Gansu Provincial People's Hospital, Lanzhou, 730000, China., Department of Stomatology, The Affiliated Hospital of Xi'an Medical College, Qindu Town, Xi'an, 710000, China., Department of Oral and Maxillofacial Surgery, Gansu Provincial People's Hospital, Lanzhou, 730000, China. Electronic address: .

Abstract:  Oral squamous cell carcinoma (OSCC) is known as one of the most common cancer influencing the head and neck region. However, the molecular mechanisms revealing OSCC progression is largely unclear. Aurora kinase A (AURKA) is a serine-threonine kinase that functions in mitotic spindle formation and chromosome segregation, and is associated with the progression of human cancers. But its role in regulating OSCC development has not yet been investigated. In the study, we found that AURKA expression was up-regulated in OSCC cell lines and tumor specimens from patients. OSCC patients with high expression of AURKA exhibited a significant decreased overall survival rate. In vitro, AURKA knockdown markedly reduced the proliferation, migration and invasion of OSCC cells using cell counting kit-8 (CCK-8), EdU, colony formation and transwell analysis. EMT was suppressed by AURKA silence, as evidenced by the up-regulated expression of E-cadherin and down-regulated Vimentin in OSCC cells. In addition, apoptosis was markedly induced by AURKA inhibition through promoting the expression of cleaved Caspase-3 and poly (ADP)-ribose polymerase (PARP). Reactive oxygen species (ROS) production was also markedly enhanced in AURKA-knockdown OSCC cells. Importantly, we found that repressing ROS generation using its scavenger of n-acetylcysteine (NAC) significantly abolished AURKA silence-induced apoptosis, accompanied with restored proliferation and EMT. In vivo, AURKA knockdown notably inhibited tumor growth. Therefore, knockdown of AURKA suppressed cell proliferation, migration and invasion, and also induced apoptosis and ROS generation in OSCC possibly via the production of ROS, demonstrating that AURKA inhibition might represent a novel therapeutic target for the prevention of OSCC. 

Retracted: No

PubPeer comments:
 Figure 3A. * Cyan boxes: The 6, 9, and 12% graphs look very similar. Do the authors still have a higher resolution version to share, please? ![file] ,
Nonsense-mediated decay serves as a general viral restriction mechanism in plants
Authors: Shahinez Garcia
Olivier Voinnet
Damien Garcia
Journal: Cell Host & Microbe (2014)
Discipline: MICROBIOLOGY
Keywords: RNA viruses; host restriction; RNA silencing; Potato virus X; genetic attenuation
Affiliations: Institut de Biologie Moléculaire des Plantes (IBMP), Centre National de la Recherche Scientifique, UPR 2357, 67084 Strasbourg, France. Electronic address: ., Institut de Biologie Moléculaire des Plantes (IBMP), Centre National de la Recherche Scientifique, UPR 2357, 67084 Strasbourg, France., Institut de Biologie Moléculaire des Plantes (IBMP), Centre National de la Recherche Scientifique, UPR 2357, 67084 Strasbourg, France; Swiss Federal Institute of Technology Zurich, Department of Biology, Universitätstrasse 2, 8092 Zürich, Switzerland. Electronic address: .

Abstract:  (+)strand RNA viruses have to overcome various points of restriction in the host to establish successful infection. In plants, this includes RNA silencing. To uncover additional bottlenecks to RNA virus infection, we genetically attenuated the impact of RNA silencing on transgenically expressed Potato virus X (PVX), a (+)strand RNA virus that replicates in Arabidopsis. A genetic screen in this sensitized background uncovered how nonsense-mediated decay (NMD), a host RNA quality control mechanism, recognizes and eliminates PVX RNAs with internal termination codons and long 3' UTRs. NMD also operates in natural infection contexts, and while some viruses have evolved genome expression strategies to overcome this process altogether, the virulence of NMD-activating viruses entails their ability to directly suppress NMD or to promote an NMD-unfavorable cellular state. These principles of induction, evasion, and suppression define NMD as a general viral restriction mechanism in plants that also likely operates in animals. 

Retracted: No

PubPeer comments:
 In Figure 2G, SD466 and SD975 xWT Col panels are identical images. ![file] ,
The FDA-approved drug ivermectin inhibits the replication of SARS-CoV-2 in vitro
Authors: Julian D Druce
Mike G Catton
David A Jans
Kylie M Wagstaff
Leon Caly
Journal: Antiviral Research (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Clinical trials; COVID-19; Ivermectin; Anti-viral activity; SARS-CoV-2
Affiliations: Victorian Infectious Diseases Reference Laboratory, Royal Melbourne Hospital, At the Peter Doherty Institute for Infection and Immunity, Victoria, 3000, Australia., Biomedicine Discovery Institute, Monash University, Clayton, Vic, 3800, Australia., Biomedicine Discovery Institute, Monash University, Clayton, Vic, 3800, Australia. Electronic address: .

Abstract:  Although several clinical trials are now underway to test possible therapies, the worldwide response to the COVID-19 outbreak has been largely limited to monitoring/containment. We report here that Ivermectin, an FDA-approved anti-parasitic previously shown to have broad-spectrum anti-viral activity in vitro, is an inhibitor of the causative virus (SARS-CoV-2), with a single addition to Vero-hSLAM cells 2 h post infection with SARS-CoV-2 able to effect ~5000-fold reduction in viral RNA at 48 h. Ivermectin therefore warrants further investigation for possible benefits in humans. 

Retracted: No

PubPeer comments:
 The Gu03b2 bands in Figure 2B (red box) were similar to the Gu03b2 bands in Figure 5B (red box) . ![file] ,
Application of Multislice Spiral CT Imaging Technology in the Diagnosis of Patients with Chest Sarcoidosis
Authors: Hong-Fei Ma
Liang Chen
Journal: Journal of Healthcare Engineering (2021)
Discipline: Multidisciplinary
Keywords: MSCT; dynamic enhancement scanning; solitary nodules; chest; CT values
Affiliations: The First Hospital of Jilin University, Changchun, Jilin Province 130012, China

Abstract:  Objective: To study the qualitative value of multislice spiral CT (MSCT) dynamic enhancement scanning for solitary nodules (SPN) of the chest. Methods: In this paper, 40 cases of chest nodules (including 25 cases of malignant nodules, 8 cases of inflammatory nodules, and 7 cases of benign nodules) were first scanned to determine the scope of nodules. At the two rates of 5 ml/s and 3 ml/s, CT dynamic enhancement scans were performed at the center of the nodule, and the CT values, peak enhancement (PH) and peak time (PT) before and after SPN enhancement, were recorded. It is mainly strengthened, with 80% (20/25) of net added value between 20 and 60 Hu, and 20% (5/25) &gt;60 Hu or &lt;20 Hu. The enhancement peak and peak time are (31.31 ± 10.62) Hu and 45 s, respectively. The time-density curve (T-DC) showed a slowly rising type; the inflammatory nodules were mainly severely strengthened, with a net increase of &gt;40 Hu. The enhancement peak value is (49.25 ± 12.44) Hu, and the peak time is 80 s and 140 s. There is a characteristic of rising and falling and then rising in the curve. Conclusion: Multislice spiral CT dynamic enhancement scan reflects the dynamic characteristics of chest nodular blood flow, which can be used to noninvasively evaluate and diagnose SPN. 

Retracted: No

PubPeer comments:
 This paper contains 8 items in the reference list, of which 4 are associated with Shaofei Wu and all irrelevant. ![file] ![file] ![file] ,