PReD-Bench/PRed-Bench huggingface dataset:
FAT10 promotes the invasion and migration of breast cancer cell through stabilization of ZEB2
Authors: Yan Zhang
Shixin Yang
Qianwen Ouyang
Yufeng Zou
Wensong Wei
Wenlong Yang
Journal: Biochemical and Biophysical Research Communications (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Breast cancer; EMT; FAT10; Migration; Ubiquitination
Affiliations: Department of Breast Surgery, The Third Hospital of Nanchang, Jiangxi Provincial-Key-Laboratory for Breast Diseases, Jiangxi Province, 330006, China., Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD, USA., Department of Infectious Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, 330006, China. Electronic address: .

Abstract:  FAT10, an ubiquitin-like protein, functions as a potential tumor promoter in several caners. However, the function and clinical significance of FAT10 in breast cancer (BC) remains unclear. Here, we found that high FAT10 expression was detected frequently in primary BC tissues, and was closely associated with malignant phenotype and shorter survival among the BC patients. Multivariate analyses also revealed that FAT10 overexpression was independent prognostic factors for poor outcome of patients with BC. Function assay demonstrated that FAT10 knockdown significantly inhibited the metastasis abilities and the epithelial-mesenchymal transition (EMT) of breast cancer cell. Further investigation revealed that FAT10 directly bound ZEB2 and decreased its ubiquitination to enhance the protein stability of ZEB2 in BC cells. Moreover, our data shown that the pro-metastasis effect of FAT10 in BC is partially dependent on ZEB2 enhancement. Collectively, our data suggest that FAT10 plays a crucial oncogenic role in BC metastasis, and we provide a novel evidence that FAT10 may be serve as a prognostic and therapeutic target for BC patients. 

Retracted: No

PubPeer comments:
 Figure 2E appears to have two images which overlap. Also some of the western blots in this paper seem to have no background noise, see the Tubulin band in Figure 1C below as an example. Could the authors please provide the original uncropped scan? *** ![file] *** ![file] ,
A fully recombinant ELISA using in vivo biotinylated antibody fragments for the detection of potato leafroll virus
Authors: Lesley Torrance
Ahmad Al-Mrabeh
Graham Cowan
Angelika Ziegler
Journal: Journal of virological methods (2009)
Discipline: MICROBIOLOGY
Keywords: recombinant antibody fusion protein; V3HCL; potato leafroll virus; PLRV; biotin labeling
Affiliations: Plant Pathology Programme, Scottish Crop Research Institute, Invergowrie, Dundee DD2 5DA, Scotland, UK.

Abstract:  A recombinant antibody fusion protein, V3HCL, which was shown previously to have specific reactivity for potato leafroll virus (PLRV), was labeled with biotin using standard chemical coupling procedures and by an in vivo method. The in vivo method proved superior giving reproducible V3HCL-biotin preparations. A fully recombinant ELISA was devised incorporating V3HCL, V3HCL-biotin and streptavidin alkaline phosphatase conjugate. This assay gave comparable results for PLRV detection in potato to an assay based on immunoglobulins. The V3HCL-biotin preparations were stable and retained specific activity for more than 1 year when stored at 4 degrees C or -20 degrees C. The results demonstrate that scFv reagents derived from synthetic phage display platforms can provide effective alternatives to assays incorporating immune reagents. 

Retracted: No

PubPeer comments:
 Fig1. Blots in general have unusually white backgrounds, two of them are duplicated and there seems to be a band cut off. Fig1.D is whole cell extract with no anti-histadine antibody, Fig 1.H is periplasmic extracts with no streptavidin antibody. Yet both these blots appear to be the same under high threshold (red boxes) albeit with slightly different contrasts. Blue arrow indicates probable band truncation in blot G, with right most part of blot being very clean even under high threshold. ![file] ,
Tumor Arrests DN2 to DN3 Pro T Cell Transition and Promotes Its Conversion to Thymic Dendritic Cells by Reciprocally Regulating Notch1 and Ikaros Signaling
Authors: Ipsita Guha
Nilanjan Ganguly
Subrata Majumdar
Shayani Dasgupta
Arathi Nair
Walter J Storkus
Partha Nandi
Divanshu Shukla
Bhaskar Saha
Ashok Patidar
Sweta Ghosh
Akata Saha
Rathindranath Baral
Anamika Bose
Avishek Bhuniya
Journal: Frontiers in Immunology (2020)
Discipline: IMMUNOLOGY
Keywords: Cancer; DC; DN2b; IL-10; T cell
Affiliations: Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), Kolkata, India., Department of Pathogenesis and Cell Responses, National Centre for Cell Sciences, Pune, India., Department of Molecular Medicine, Bose Institute, Kolkata, India., Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.

Abstract:  Tumor progression in the host leads to severe impairment of intrathymic T-cell differentiation/maturation, leading to the paralysis of cellular anti-tumor immunity. Such suppression manifests the erosion of CD4+CD8+ double-positive (DP) immature thymocytes and a gradual increase in CD4-CD8- double negative (DN) early T-cell progenitors. The impact of such changes on the T-cell progenitor pool in the context of cancer remains poorly investigated. Here, we show that tumor progression blocks the transition of Lin-Thy1.2+CD25+CD44+c-KitlowDN2b to Lin-Thy1.2+CD25+CD44-c-Kit-DN3 in T-cell maturation, instead leading to DN2-T-cell differentiation into dendritic cells (DC). We observed that thymic IL-10 expression is upregulated, particularly at cortico-medullary junctions (CMJ), under conditions of progressive disease, resulting in the termination of IL-10Rhigh DN2-T-cell maturation due to dysregulated expression of Notch1 and its target, CCR7 (thus restricting these cells to the CMJ). Intrathymic differentiation of T-cell precursors in IL-10-/- mice and in vitro fetal thymic organ cultures revealed that IL-10 promotes the interaction between thymic stromal cells and Notch1low DN2-T cells, thus facilitating these DN2-T cells to differentiate toward CD45+CD11c+MHC-II+ thymic DCs as a consequence of activating the Ikaros/IRF8 signaling axis. We conclude that a novel function of thymically-expressed IL-10 in the tumor-bearing host diverts T-cell differentiation toward a DC pathway, thus limiting the protective adaptive immune repertoire. 

Retracted: No

PubPeer comments:
 Figure 1E contains a duplicated FACS plot ![file] ,
Alpha-ketoglutarate promotes skeletal muscle hypertrophy and protein synthesis through Akt/mTOR signaling pathways
Authors: Qingyan Jiang
Yaqiong Xu
Yuanyuan Jing
Canjun Zhu
Xiaotong Zhu
Songbo Wang
Ping Gao
Gang Shu
Yongliang Zhang
Yexian Yuan
Xingcai Cai
Lina Wang
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: Skeletal muscle weight loss; fiber size; protein content; Alpha-ketoglutarate (AKG); protein metabolism
Affiliations: National Engineering Research Center for Breeding Swine Industry, College of Animal Science, South China Agricultural University, Guangzhou, Guangdong, 510642, China., ALLTECH-SCAU Animal Nutrition Control Research Alliance, South China Agricultural University, Guangzhou 510642, PR China.

Abstract:  Skeletal muscle weight loss is accompanied by small fiber size and low protein content. Alpha-ketoglutarate (AKG) participates in protein and nitrogen metabolism. The effect of AKG on skeletal muscle hypertrophy has not yet been tested, and its underlying mechanism is yet to be determined. In this study, we demonstrated that AKG (2%) increased the gastrocnemius muscle weight and fiber diameter in mice. Our in vitro study also confirmed that AKG dose increased protein synthesis in C2C12 myotubes, which could be effectively blocked by the antagonists of Akt and mTOR. The effects of AKG on skeletal muscle protein synthesis were independent of glutamate, its metabolite. We tested the expression of GPR91 and GPR99. The result demonstrated that C2C12 cells expressed GPR91, which could be upregulated by AKG. GPR91 knockdown abolished the effect of AKG on protein synthesis but failed to inhibit protein degradation. These findings demonstrated that AKG promoted skeletal muscle hypertrophy via Akt/mTOR signaling pathway. In addition, GPR91 might be partially attributed to AKG-induced skeletal muscle protein synthesis. 

Retracted: Yes

PubPeer comments:
 Figure 7E has several images that appear to share the same origin. Two overlap, one is flipped (see common features marked in green), all appear to have different tint. *** Closeup ![file] *** Full figure ![file] ,
Salmon provides fast and bias-aware quantification of transcript expression
Authors: Rafael A Irizarry
Michael I Love
Geet Duggal
Rob Patro
Carl Kingsford
Journal: Nature methods (2017)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Salmon; transcript abundance; RNA-seq reads; dual-phase parallel inference algorithm; bias models
Affiliations: Department of Computer Science, Stony Brook University, Stony Brook, New York, USA., DNAnexus, Mountain View, California, USA., Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Cambridge, Massachusetts, USA., Department of Biostatistics, Harvard T.H. Chan School of Public Health, Cambridge, Massachusetts, USA., Computational Biology Department, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.

Abstract:  We introduce Salmon, a lightweight method for quantifying transcript abundance from RNA-seq reads. Salmon combines a new dual-phase parallel inference algorithm and feature-rich bias models with an ultra-fast read mapping procedure. It is the first transcriptome-wide quantifier to correct for fragment GC-content bias, which, as we demonstrate here, substantially improves the accuracy of abundance estimates and the sensitivity of subsequent differential expression analysis. 

Retracted: No

PubPeer comments:
 They show increased alpha ENaC mRNA and possibly protein. However, there are no data addressing whether the differences in inflammation or alveolar fluid clearance are ENaC-dependent (e.g. a control with an ENaC blocker or genetic model). PPAR gamma increases expression of hundreds of targets and has well-known anti-inflammatory effects. Inoue et al (2003) Eur J Pharmacol found that, in mice with LPS-induced pulmonary edema, the PPAR gamma activation with 15-PGJ2 increased lung wet-dry weight and inflammatory infiltrate. Different PPAR gamma agonist and different mice, but authors did not discuss their differences with this paper. ,
Identification of a tumor-suppressive human-specific microRNA within the FHIT tumor-suppressor gene
Authors: Fang Yu
Ya Wang
I King Jordan
Wuju Li
Xiaomin Ying
Walter J Curran
Xiang Wang
Xiaofei Zheng
Jittima Piriyapongsa
Wooi Loon Ng
Yazhuo Li
Jian Wang
Po Zhao
Shuofeng Hu
Chenguang Wang
Baocheng Hu
Hongyan Wang
Jipo Sheng
Journal: Cancer research (2014)
Discipline: CLINICAL MEDICINE
Keywords: tumor-suppressor gene; FHIT; apoptosis; reactive oxygen species; bioinformatics
Affiliations: Authors' Affiliations: Department of Medical Molecular Biology, Beijing Institute of Biotechnology; Center of Computational Biology, Beijing Institute of Basic Medical Sciences; Department of Pathology, Chinese PLA General Hospital; Department of Biochemistry and Molecular Biology, Beijing Institute of Radiation Medicine, Beijing, China; Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University; School of Biology, Georgia Institute of Technology, Atlanta, Georgia; Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania; and Genome Institute, National Center for Genetic Engineering and Biotechnology, Pathumthani, Thailand.

Abstract:  Loss or attenuated expression of the tumor-suppressor gene FHIT is associated paradoxically with poor progression of human tumors. Fhit promotes apoptosis and regulates reactive oxygen species; however, the mechanism by which Fhit inhibits tumor growth in animals remains unclear. In this study, we used a multidisciplinary approach based on bioinformatics, small RNA library screening, human tissue analysis, and a xenograft mouse model to identify a novel member of the miR-548 family in the fourth intron of the human FHIT gene. Characterization of this human-specific microRNA illustrates the importance of this class of microRNAs in tumor suppression and may influence interpretation of Fhit action in human cancer. 

Retracted: No

PubPeer comments:
 Figure 2B. Much more similar than you would expect. https: imgur.com qjHDhhl Figure 5B.u00a0Much more similar than you would expect.u00a0u00a0 https: imgur.com l9BRgOG , 
 Figure 2B. Left side actin panel. Much more similar than you would expect. https: imgur.com MR8lwh3 , 
 #1 Figure 5B. Much more similar than you would expect. https: imgur.com tFmDhuz ,
Circular RNA circ_0074026 indicates unfavorable prognosis for patients with glioma and facilitates oncogenesis of tumor cells by targeting miR‐1304 to modulate ERBB4 expression
Authors: Peng Xie
Pengyu Wang
Xiaojuan Liu
Yongxuan Zhan
Yongli Li
Minghui Chen
Mingli Liu
Yan Feng
Hongjun Wang
Journal: Journal of Cellular Physiology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ERBB4; circ_0074026; circular RNA; glioma; miR-1304.
Affiliations: Department of Neurosurgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China., Department of Hematological Oncology, The First Hospital of Harbin, Harbin, China.

Abstract:  Glioma (GM) is a common malignancy all over the world. A novel circular RNA (circRNA), circ_0074026, has been documented to be upregulated in GM tissues than that of normal counterparts, as confirmed by circRNA microarray. However, the biological mechanism of circ_0074026 is still unreported in GM. The expression of circ_0074026 in GM specimens or cells was detected by quantitative real-time polymerase chain reaction. Fisher's exact test was utilized to evaluate the clinical relevance of circ_0074026 in patients with GM. Kaplan-Meier and Cox regression analysis were used to estimate the prognostic value of circ_0074026. Cell counting kit-8 (CCK-8), acridine orange/ethidium bromide double fluorescence staining, flow cytometry, wound healing, and Transwell assays were used to detect the malignant behaviors of GM cells including cell growth, apoptosis, migration, and invasion. CCK-8 and flow cytometric experiments were utilized to evaluate whether circ_0074026 had a side effect on normal human astrocyte cells. The interaction between miR-1304 and circ_0074026 or ERBB4 3'-untranslated region (3'-UTR) was predicted with circular RNA Interactome and TargetScan, respectively, and then confirmed by the dual-luciferase reporter test. The levels of circ_0074026 were both apparently increased in GM samples and cells. The elevated expression of circ_0074026 was linked to patients' tumor size, WHO grade, disease-free survival, and overall survival. The depletion of circ_0074026 can block cell growth, migration, invasion, and impel cell apoptosis in the LN229 cell line. However, ectopically expressed circ_0074026 caused the opposite effect in the U251 cell line. The following dual-luciferase reporter assay demonstrated that miR-1304 interacted with circ_0074026 and ERBB4 3'-UTR. Furthermore, the rescue assay indicated that circ_0074026 modulated ERBB4 to promote tumor progression by regulating miR-1304. Thus, a novel regulatory pathway may provide a new therapeutic target for patients with GM. 

Retracted: No

PubPeer comments:
 Figure 6D: * Red boxes: One of the panels looks very similar to a panel in another figure by Yi Xu et al, Oncotarget (2017), DOI: 10.18632 oncotarget.19502 - https: pubpeer.com publications E03D4E3C0EF54498FA06B71E6C20FC Note that the two panels represent very different experiments and cell lines. Can the authors please provide an explanation? Both research groups are affiliated with the Second Affiliated Hospital of Harbin Medical University. ![file] ,
On the other hand: dummy hands and peripersonal space
Authors: Tamar R Makin
H Henrik Ehrsson
Nicholas P Holmes
Journal: Behavioural Brain Research (2008)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: hands; sensory information; multisensory interactions; peripersonal space; neurophysiological
Affiliations: Department of Neurobiology, Life Sciences Institute, Hebrew University, Jerusalem 91904, Israel. 

Abstract:  Where are my hands? The brain can answer this question using sensory information arising from vision, proprioception, or touch. Other sources of information about the position of our hands can be derived from multisensory interactions (or potential interactions) with our close environment, such as when we grasp or avoid objects. The pioneering study of multisensory representations of peripersonal space was published in Behavioural Brain Research almost 30 years ago [Rizzolatti G, Scandolara C, Matelli M, Gentilucci M. Afferent properties of periarcuate neurons in macaque monkeys. II. Visual responses. Behav Brain Res 1981;2:147-63]. More recently, neurophysiological, neuroimaging, neuropsychological, and behavioural studies have contributed a wealth of evidence concerning hand-centred representations of objects in peripersonal space. This evidence is examined here in detail. In particular, we focus on the use of artificial dummy hands as powerful instruments to manipulate the brain's representation of hand position, peripersonal space, and of hand ownership. We also review recent studies of the 'rubber hand illusion' and related phenomena, such as the visual capture of touch, and the recalibration of hand position sense, and discuss their findings in the light of research on peripersonal space. Finally, we propose a simple model that situates the 'rubber hand illusion' in the neurophysiological framework of multisensory hand-centred representations of space. 

Retracted: No

PubPeer comments:
 This paper was criticised as part of a self-reflection posted on Twitter on 2nd-3rd April, 2021 (twitter TheHandLab status 1377760796130869248) Criticism: Like all of my reviews until ~2019, this was a selective, narrative review, opinion, model of how the Rubber Hand Illusion may relate to Peripersonal Space. The model we proposed was somewhat ad-hoc, largely meant as a commentary on a previous model proposed by Manos Tsakiris. I would now require that a systematic review of the literature is required before generating such a model. ,
Alpinumisoflavone suppresses tumour growth and metastasis of clear-cell renal cell carcinoma
Authors: Tingting Wang
Tianhui Wu
Lei Chu
Yuhua Jiang
Jie You
Journal: American journal of cancer research (2017)
Discipline: CLINICAL MEDICINE
Keywords: Alpinumisoflavone; RLIP76; clear cell renal cell carcinoma; miR-101.
Affiliations: Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of MedicineShanghai 200011, China., Tumor Hospital of QingdaoShandong 266042, China., Qingdao 5th People's HospitalQingdao 266002, Shandong, China.

Abstract:  Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer. The present study is aimed to investigate the role of alpinumisoflavone (AIF), a naturally occurring flavonoid compound, in ccRCC and the underlying mechanism. In this study, miR-101 has been identified as a novel therapeutic target, which exerts anti-tumor effect on ccRCC by directly targeting RLIP76. Moreover, our results showed that AIF was able to increase the expression of miR-101 by suppressing Akt signalling. Our findings in this study provided experimental evidence that AIF has the potential to be used as an agent in the treatment of ccRCC. 

Retracted: No

PubPeer comments:
 ![file] Plagiarising [a comment by Elisabeth Bik] : This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels. Despite these similarities, these papers are authored by researchers from different departments and institutes, with almost no overlap in authors. The list of these papers is available here: https: docs.google.com spreadsheets d 1KXqTAyl4j-jVorFPMD2XRpr76LcIKJ0CVyIvRj0exYQ edit?usp=sharing A more detailed description of this set of papers, suspected to all be generated by a common source, a paper mill , can be found here: - https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers (January 2020) - https: scienceintegritydigest.com 2020 02 21 the-tadpole-paper-mill (February 2020) The same paper mill has been described in these papers: - Jana Christopher - Systematic fabrication of scientific images revealed - FEBS Letters (2018) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13201 - Jennifer A Byrne and Jana Christopher - Digital magic, or the dark arts of the 21st centuryu2014how can journals and peer reviewers detect manuscripts and publications from paper mills? - FEBS Letters (2020) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13747 ,
Influence of the behaviour pattern on the nocebo response of healthy volunteers
Authors: F Raybaud
M D Drici
P Gustovic
C De Lunardo
P Iacono
Journal: British journal of clinical pharmacology (1995)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: nocebo effect; personality type; Bortner Rating Scale; subjective side effects; placebo administration
Affiliations: Clinical Pharmacology Center, University of Nice-Sophia Antipolis, France.

Abstract:  The occurrence of a nocebo effect after placebo administration to healthy volunteers in a Phase I trial was analysed according to their type of personality (Bortner Rating Scale). More subjects with a behaviour pattern A (competitive and aggressive) (50%) described subjective side effects of the placebo than type B subjects (17%, P = 0.03). The volunteers who had nocebo effect had a higher Bortner score (BS) than did placebo non-responsive subjects (P = 0.05). The BS was 205 for paramedical staff, 189 for medical and dentistry students, 173 for non-science students and 161 for science students (P &lt; 0.04). The nocebo response was not statistically correlated with professional status. These results suggest that volunteer's type of personality might influence the reporting of subjective symptoms after placebo, and therefore impair the evaluation of new drugs in Phase I clinical trials. 

Retracted: No

PubPeer comments:
 # **Figure 3C** ![file] , 
 In Figure3 F, the Alpha-Tubulin panel appears to look very similar to the Alpha-Tubulin panel in Figure5 C, although they are representing different experiments done at different experimental stage. # Fig. 3 F and Fig. 5 C # ![file] ,
Baicalein suppresses hypoxia-induced HIF-1alpha protein accumulation and activation through inhibition of reactive oxygen species and PI 3-kinase/Akt pathway in BV2 murine microglial cells
Authors: Jinhwa Lee
Young Taek Oh
Wonchae Choe
Insug Kang
Keun Young Hwang
Hana Yoon
Hocheol Kim
Journal: Neuroscience Letters (2008)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Hypoxia; Inflammation; Microglia; Ischemia; HIF-1
Affiliations: Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.

Abstract:  Hypoxia induces an inflammatory activation of microglia during cerebral ischemia. The transcription factor of hypoxia-inducible genes hypoxia-inducible factor-1 (HIF-1) is known to be involved in inflammation and immune response. Although baicalein (BE), a flavonoid, is shown to have anti-inflammatory effects and attenuate ischemic injury, its action mechanism is not understood well. Thus, we examined effect of BE on hypoxia-induced HIF-1 activation and its signaling mechanism in BV2 microglial cells. BE inhibited hypoxia-induced HIF-1alpha protein accumulation and HIF-1 transcriptional activation. Consistently, BE suppressed hypoxia-induced expression of hypoxia responsive genes, iNOS, COX-2, and VEGF. We then showed that BE inhibited hypoxia-induced phosphorylation of Akt but not that of ERK and p38. Moreover, BE inhibited hypoxia-induced PI 3-kinase activation. Finally, we showed that BE inhibited hypoxia-induced ROS generation, and an antioxidant N-acetylcysteine reduced hypoxia-induced HIF-1alpha and iNOS protein expression and PI 3-kinase/Akt activation in BV2 microglia. Taken together, these results suggest that BE suppresses hypoxia-induced HIF-1alpha protein and activation as well as expression of hypoxia responsive genes by inhibiting ROS and PI 3-kinase/Akt pathway in BV2 microglia. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] , 
 ![file] ,
MicroRNA‑10a suppresses breast cancer progression via PI3K/Akt/mTOR pathway
Authors: Tingting Lou
Kongliang Ke
Journal: Oncology Letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: breast cancer; microRNA-10a; mitochondrial apoptotic pathway; phosphoinositide-3/protein kinase B/mammalian target of rapamycin.
Affiliations: Department of General Surgery, Ningbo First Hospital, Ningbo, Zhejiang 315010, P.R. China., Department of Breast Surgery, Ningbo Hangzhou Bay Hospital, Ningbo, Zhejiang 315336, P.R. China.

Abstract:  Previous studies have demonstrated that microRNA-10a (miR-10a) regulates various opposing biological functions in breast cancer. The aim of the present study was to investigate the exact functions of miR-10a in the pathogenesis of breast cancer. miR-10a expression was initially detected in two human breast cancer cell lines, MCF-7 and MDA-MB-231 and a normal human mammary epithelial cell line MCF-10A. The proliferation, migration and apoptosis of breast cancer cells were analyzed using MTT assays, Transwell assays and flow cytometry, respectively, following transfection of MCF-7 and MDA-MB-231 cells with an miR-10a mimic or anti-miR-10a. The expression of phosphorylated (p-)protein kinase B (Akt), p-mammalian target of rapamycin (p-mTOR), p-ribosomal protein S6 kinase β-1 (p-p70S6K), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (PIK3CA), Cytochrome C (Cyt C), B-cell lymphoma 2 (Bcl-2), BCL-2 associated X, apoptosis regulator (Bax), and cleaved caspase-3 were analyzed by western blotting. The migration of MCF-7 cells pretreated with an mTOR inhibitor CCI-779, was detected using a Transwell assay. Relative miR-10a expression was significantly elevated in MDA-MB-231 breast cancer cells and was at its highest levels in MCF-7 cells. Transfection with the miR-10a mimic significantly inhibited proliferation and migration, and promoted the apoptosis of breast cancer cells. Furthermore, upregulation of miR-10a markedly suppressed the levels of p-Akt, p-mTOR, p-p70S6K, and PIK3CA, and increased the expression of Cyt C, cleaved caspase-3, and the ratio of Bax/Bcl-2. Anti-miR-10a had the opposite effects. In addition, CCI-779 reversed the effect of anti-miR-10a on the migration of MCF-7 cells in a dose-dependent manner. In conclusion, miR-10a is downregulated in high aggressive breast cancer cells. miR-10a inhibited the proliferation and migration, and promoted apoptosis of breast cancer cells via phosphoinositide/Akt/mTOR signaling, and the mitochondrial apoptotic pathway. 

Retracted: No

PubPeer comments:
 Fig 2C.  The apoptosis of MCF-7 and MDA-MB-231 cells transfected with miR-10a was analyzed by flow cytometry . ![file] Could the authors comment on the unexpected similarities between the lower-right panel (in the dark gray box) and a grey-boxed panel in Fig 2a of [Zhang (2019)] ? ![] ![file] ,
The role of kinin receptors in preventing neuroinflammation and its clinical severity during experimental autoimmune encephalomyelitis in mice
Authors: João B Calixto
Allisson F Bento
Marianne N Manjavachi
Eliziane S Patrício
João B Pesquero
Rafael C Dutra
Daniela F P Leite
Cláudia P Figueiredo
Journal: PLoS ONE (2011)
Discipline: Multidisciplinary
Keywords: Multiple sclerosis; MS; kinins; kinin receptor; EAE
Affiliations: Department of Pharmacology, Centre of Biological Sciences, Universidade Federal de Santa Catarina, Florianópolis, Santa Catarina, Brazil.

Abstract:  Background: Multiple sclerosis (MS) is a demyelinating and neuroinflammatory disease of the human central nervous system (CNS). The expression of kinins is increased in MS patients, but the underlying mechanisms by which the kinin receptor regulates MS development have not been elucidated. Methodology/principal findings: Experimental autoimmune encephalomyelitis (EAE) was induced in female C57BL/6 mice by immunization with MOG(35-55) peptide emulsified in complete Freund's adjuvant and injected with pertussis toxin on day 0 and day 2. Here, we report that blockade of the B(1)R in the induction phase of EAE markedly suppressed its progression by interfering with the onset of the immune response. Furthermore, B(1)R antagonist suppressed the production/expression of antigen-specific T(H)1 and T(H)17 cytokines and transcription factors, both in the periphery and in the CNS. In the chronic phase of EAE, the blockade of B(1)R consistently impaired the clinical progression of EAE. Conversely, administration of the B(1)R agonist in the acute phase of EAE suppressed disease progression and inhibited the increase in permeability of the blood-brain barrier (BBB) and any further CNS inflammation. Of note, blockade of the B(2)R only showed a moderate impact on all of the studied parameters of EAE progression. Conclusions/significance: Our results strongly suggest that kinin receptors, mainly the B(1)R subtype, play a dual role in EAE progression depending on the phase of treatment through the lymphocytes and glial cell-dependent pathways. 

Retracted: No

PubPeer comments:
 Figure 2E: More similar than expected ![file] Figure 3: More similar than expected, could authors check please? ![file] ,
Members of the H3K4 trimethylation complex regulate lifespan in a germline-dependent manner in C. elegans
Authors: Or Gozani
Dena S Leeman
Max R Banko
Eric L Greer
Shuo Han
Anne Brunet
Travis J Maures
Géraldine S Maro
Anna G Hauswirth
Erin M Green
Journal: Nature (2010)
Discipline: Multidisciplinary
Keywords: plasticity; ageing; longevity; epigenetically; chromatin state
Affiliations: Department of Genetics, Stanford University, 300 Pasteur Drive, Stanford, California 94305, USA.

Abstract:  The plasticity of ageing suggests that longevity may be controlled epigenetically by specific alterations in chromatin state. The link between chromatin and ageing has mostly focused on histone deacetylation by the Sir2 family, but less is known about the role of other histone modifications in longevity. Histone methylation has a crucial role in development and in maintaining stem cell pluripotency in mammals. Regulators of histone methylation have been associated with ageing in worms and flies, but characterization of their role and mechanism of action has been limited. Here we identify the ASH-2 trithorax complex, which trimethylates histone H3 at lysine 4 (H3K4), as a regulator of lifespan in Caenorhabditis elegans in a directed RNA interference (RNAi) screen in fertile worms. Deficiencies in members of the ASH-2 complex-ASH-2 itself, WDR-5 and the H3K4 methyltransferase SET-2-extend worm lifespan. Conversely, the H3K4 demethylase RBR-2 is required for normal lifespan, consistent with the idea that an excess of H3K4 trimethylation-a mark associated with active chromatin-is detrimental for longevity. Lifespan extension induced by ASH-2 complex deficiency requires the presence of an intact adult germline and the continuous production of mature eggs. ASH-2 and RBR-2 act in the germline, at least in part, to regulate lifespan and to control a set of genes involved in lifespan determination. These results indicate that the longevity of the soma is regulated by an H3K4 methyltransferase/demethylase complex acting in the C. elegans germline. 

Retracted: No

PubPeer comments:
 Readers should become aware of a recent preprint that calls into question part of the conclusions of the study by Greer et al., 2010 entitled Loss of SET1 COMPASS methyltransferase activity reduces lifespan and fertility in Caenorhabditis elegans . https: www.biorxiv.org content 10.1101 2021.06.07.447374v1.full.pdf From the text: An earlier study reported that the lifespan of set-2(ok952) mutant animals was approximately 20% longer than that of wild-type animals (34), which contrasts with the observations in the present study (...) Taken together, these data and the results of the present study argue against a simple model in which H3K4 methylation and demethylation play opposing roles in lifespan regulation (34). ,
RETRACTED ARTICLE: Site Specific Interaction Between TiO2 Nanoparticles and Phenanthrimidazole—A First Principles Quantum Mechanical Study
Authors: Periyasamy Ramanathan
Jayaraman Jayabharathi
Venugopal Thanikachalam
Chockalingam Karunakaran
Journal: Journal of Fluorescence (2015)
Discipline: CHEMISTRY
Keywords: nanomaterials; bioactive molecules; fluorophore; imidazole; TiO2 nanocrystals
Affiliations: Department of Chemistry, Annamalai University, Annamalainagar, 608 002, Tamilnadu, India, .

Abstract:  Understanding the interaction between the nanomaterials and bioactive molecules are of current interest due to the potential application of nanomaterial in biomedical field. The structural, electronic and optical properties of newly synthesised fluorophore 2-(4-methoxynaphthalen-1-yl)-1-phenyl-1H-phenanthro[9.10-d]imidazole have been investigated in detail. The imidazole absorbs strongly on the surface of TiO2 nanocrystals probably because of the chemical affinity of azomethine nitrogen atom of the imidazole, resulting in lowering the HOMO and LUMO energy levels. The TEM, SEM and EDX spectra confirm the adsorption of imidazole on the surface of TiO2 nanocrystals. The growth behavior and stability of small stoichiometric (TiO2)n clusters have been analysed by using density functional theory which reveals that clusters prefers three-dimensional structures. In addition, the interaction between the ground state structure of the (TiO2)n cluster and a single imidazole molecule have been studied. The calculated binding energy (Eb) and the energy gap (Eg) indicate that the imidazole molecule preferably binds to the Ti atom of the (TiO2)n clusters through its azomethine nitrogen atom; the binding energy is in range 5.24-7.89 eV. In order to understand the binding interaction with DNA docking study has been carried out. 

Retracted: Yes

PubPeer comments:
 Figure 1: the  5 Months Storage and  Heat Dried 2 d patterns are identical. Original scan: ![file] scan copied and lower pattern overlain on upper: ![file] and an expanded view of upper and lower patterns compared: ![file] ,
Effect of the cumin cyminum L. Intake on Weight Loss, Metabolic Profiles and Biomarkers of Oxidative Stress in Overweight Subjects: A Randomized Double-Blind Placebo-Controlled Clinical Trial
Authors: Ahmad Esmaillzadeh
Mohsen Taghizadeh
Mohammad Reza Memarzadeh
Zatollah Asemi
Journal: Annals of Nutrition and Metabolism (2015)
Discipline: CLINICAL MEDICINE
Keywords: cumin cyminum L.; weight loss; metabolic profiles; overweight subjects; clinical trial
Affiliations: Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran.

Abstract:  Background: The current study was performed to determine the effects of cumin cyminum L. intake on weight loss and metabolic profiles among overweight subjects. Methods: This randomized double-blind placebo-controlled clinical trial was conducted among 78 overweight subjects (male, n = 18; female, n = 60) aged 18-60 years old. Participants were randomly assigned into three groups to receive: (1) cumin cyminum L. capsule (n = 26); (2) orlistat120 capsule (n = 26) and (3) placebo (n = 26) three times a day for 8 weeks. Anthropometric measures and fasting blood samples were taken at baseline and after 8 weeks of intervention. Results: Consumption of the Cuminum cyminum L. and orlistat120 resulted in a similar significant decrease in weight (-1.1 ± 1.2 and -0.9 ± 1.5 vs. 0.2 ± 1.5 kg, respectively, p = 0.002) and BMI (-0.4 ± 0.5 and -0.4 ± 0.6 vs. 0.1 ± 0.6 kg/m(2), respectively, p = 0.003) compared with placebo. In addition, taking Cuminum cyminum L., compared with orlistat and placebo, led to a significant reduction in serum insulin levels (-1.4 ± 4.5 vs. 1.3 ± 3.3 and 0.3 ± 2.2 µIU/ml, respectively, p = 0.02), HOMA-B (-5.4 ± 18.9 vs. 5.8 ± 13.3 and 1.0 ± 11.0, respectively, p = 0.02) and a significant rise in QUICKI (0.01 ± 0.01 vs. -0.005 ± 0.01 and -0.004 ± 0.01, respectively, p = 0.02). Conclusion: Taking cumin cyminum L. for eight weeks among overweight subjects had the same effects of orlistat120 on weight and BMI and beneficial effects on insulin metabolism compared with orlistat120 and placebo. 

Retracted: No

PubPeer comments:
 ![file] ,
Targeting of GSK3β promotes imatinib-mediated apoptosis in quiescent CD34+ chronic myeloid leukemia progenitors, preserving normal stem cells
Authors: Luciana Dini
Simone De Leo
Ilaria Palamà
Michele Maffia
Emanuela de Luca
Carlo Gambacorti Passerini
Nicola Di Renzo
Giovanni Reddiconto
Addolorata Maria Luce Coluccia
Serena De Matteis
Claudia Toto
Journal: Blood (2012)
Discipline: CLINICAL MEDICINE
Keywords: BCR-ABL; GSK3β; CML; leukemia-initiating cells; MAPK
Affiliations: Hematology Unit, Vito Fazzi Hospital Azienda Sanitaria Locale Leece, Italy.

Abstract:  The targeting of BCR-ABL, a hybrid oncogenic tyrosine (Y) kinase, does not eradicate chronic myeloid leukemia (CML)-initiating cells. Activation of β-catenin was linked to CML leukemogenesis and drug resistance through its BCR-ABL-dependent Y phosphorylation and impaired binding to GSK3β (glycogen synthase kinase 3β). Herein, we show that GSK3β is constitutively Y(216) phospho-activated and predominantly relocated to the cytoplasm in primary CML stem/progenitor cells compared with its balanced active/inactive levels and cytosolic/nuclear distribution in normal cells. Under cytokine support, persistent GSK3β activity and its altered subcellular localization were correlated with BCR-ABL-dependent and -independent activation of MAPK and p60-SRC/GSK3β complex formation. Specifically, GSK3β activity and nuclear import were increased by imatinib mesylate (IM), a selective ABL inhibitor, but prevented by dasatinib that targets both BCR-ABL- and cytokine-dependent MAPK/p60-SRC activity. SB216763, a specific GSK3 inhibitor, promoted an almost complete suppression of primary CML stem/progenitor cells when combined with IM, but not dasatinib, while sparing bcr-abl-negative cells. Our data indicate that GSK3 inhibition acts to prime a pro-differentiative/apoptotic transcription program in the nucleus of IM-treated CML cells by affecting the β-catenin, cyclinD1, C-EBPα, ATF5, mTOR, and p27 levels. In conclusion, our data gain new insight in CML biology, indicating that GSK3 inhibitors may be of therapeutic value in selectively targeting leukemia-initiating cells in combination with IM but not dasatinib. 

Retracted: No

PubPeer comments:
 #1 How to account for the bands inside the yellow rectangles looking so similar in two different Blood papers Could the authors post high definition images of the full blots used to make figure 2 Blood 119:2335 (2012) here? , 
null, 
null, 
 #1 Clarification. ![file] ,
Perturbation of endoplasmic reticulum homeostasis facilitates prion replication
Authors: Claudio Soto
Claudio Hetz
Joaquín Castilla
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Prion diseases; PrP; ER stress; neurodegenerative disorders; apoptosis

Abstract:  Prion diseases are fatal and infectious neurodegenerative disorders characterized by the accumulation of an abnormally folded form of the prion protein (PrP), termed PrP(Sc). Prion replication triggers endoplasmic reticulum (ER) stress, neuronal dysfunction, and apoptosis. In this study we analyze the effect of perturbations in ER homeostasis on PrP biochemical properties and prion replication. ER stress led to the generation of a mis-folded PrP isoform, which is detergent-insoluble and protease-sensitive. To understand the mechanism by which ER stress generates PrP misfolding, we assessed the contribution of different signaling pathways implicated in the unfolded protein response. Expression of a dominant negative form of IRE1 alpha or XBP-1 significantly increased PrP aggregation, whereas overexpression of ATF4 or an active mutant form of XBP-1 and ATF6 had the opposite affect. Analysis of prion replication in vitro revealed that the PrP isoform generated after ER stress is more efficiently converted into PrP(Sc) compared with the protein extracted from untreated cells. These findings indicate that ER-damaged cells might be more susceptible to prion replication. Because PrP(Sc) induces ER stress, our data point to a vicious cycle accelerating prion replication, which may explain the rapid progression of the disease. 

Retracted: No

PubPeer comments:
 Fig. 5A: Contrast enhanced. It seems that WB: Total PrP4F4 presents differential splicing in some lanes. Could authors check this issue please? ![file] , 
 Identified by another reader. Could the authors please respond as they have elsewhere? *** ![file] , 
 https: www.uchile.cl noticias 179784 comunicado-sobre-profesor-hetz , 
 It seems that part of this panel was published in a previous study (DOI: https: doi.org 10.1523 JNEUROSCI.4090-04.2005), however, this is not referenced on the figure legends ![file] , 
 #4 If you look at the figure in the paper from 2005 and compare it to the paper of 2007, you can see the the NT and Brefeldin A pictures are the same, but in the 2007 paper the lactacystine group has been added. If you now compare the immunofluorescence colors (nuclear stain) between NT Brefeldin A to lactacystine, the colors do not match. so not only is there a duplication not noted in the manuscript, but it also looks like a new group was added to an old experiment. I would question if the panels even come from the same experiment. In fact, I did that by writing to both journal in 2009, but I never received a reply back. I guess there was no interest in correcting this blatant error. ,
Inhibition of the proteasomal function in chondrocytes down-regulates growth plate chondrogenesis and longitudinal bone growth
Authors: Shufang Wu
Francesco De Luca
Journal: Endocrinology (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: proteasome; osteoblast differentiation; bone formation; growth plate; chondrocyte proliferation
Affiliations: Section of Endocrinology and Diabetes, St. Christopher's Hospital for Children, Philadelphia, Pennsylvania 19134, USA.

Abstract:  The proteasome is a large multiprotein complex that processes intracellular proteins functioning as cell cycle regulators and transcription factors. It has been shown that the chymotryptic component of the proteasome is an important regulator of osteoblast differentiation and bone formation, with inhibitors of the proteasome increasing osteoblast differentiation and bone formation. Yet, little is known about the effects of the proteasomal activity in the growth plate. In the present study, we cultured rat metatarsal bones in the presence of proteasome inhibitor I (PSI), a known inhibitor of the chymotrypsin-like activity of the 20S proteasome. PSI suppressed growth plate chondrocyte proliferation and hypertrophy/differentiation, and induced chondrocyte apoptosis. All these cellular effects led to reduced metatarsal linear growth. In cultured chondrocytes, PSI increased the expression of beta-catenin (a negative regulator of chondrogenesis) and reduced the DNA binding of nuclear factor kappaB, a transcription factor that stimulates growth plate chondrogenesis. In conclusion, our findings suggest that the proteasomal activity facilitates growth plate chondrogenesis and, in turn, longitudinal bone growth. 

Retracted: No

PubPeer comments:
 Figure 6B. Much more similar than you would expect. https: imgur.com RvTkTcQ ,
The role of colonic mast cells and myenteric plexitis in patients with diverticular disease
Authors: Elisabetta Antonelli
Amin Titi
Gabrio Bassotti
Moris Cadei
Riccardo Nascimbeni
Vincenzo Villanacci
Luisa Lorenzi
Bruno Salerni
Stefania Manenti
Journal: International journal of colorectal disease (2013)
Discipline: CLINICAL MEDICINE
Keywords: Gut mast cells; colonic diverticular disease; surgery; mast cells; tryptase
Affiliations: Gastroenterology and Hepatology Section, Department of Clinical and Experimental Medicine, University of Perugia, Perugia, Italy. 

Abstract:  Background: Gut mast cells represent an important cell population involved in intestinal homeostasis and inflammatory processes. However, their possible role has not to date been investigated in colonic diverticular disease. Aims: This study aims to evaluate colonic mast cells in patients undergoing surgery for diverticular disease. Methods: Surgical resection samples from 27 patients undergoing surgery for diverticular disease (12 emergency procedures for severe disease and 15 elective procedures) were evaluated. The number of mast cells was assessed in the various layers by means of a specific antibody (tryptase) and compared with those evaluated in ten controls. In patients with mast cells degranulation, double immunohistochemistry, also assessing nerve fibres, was carried out. In addition, the presence of myenteric plexitis was sought. Results: Compared with controls, the number of mast cells in diverticular patients was significantly increased, both as an overall figure and in the various layers of the large bowel. In patients in whom mast cells degranulation was present, these were always closed to nerve fibres. No differences were found between the two subgroups of patients with respect to the number and distribution of mast cells; however, all patients undergoing emergency surgery (but none of those undergoing elective procedures) had myenteric plexitis, represented by lymphocytic infiltration in 67 % and eosinophilic infiltration in 33 % of cases. Conclusions: Patients with diverticular disease display an increase of mast cells in the large bowel. The presence of myenteric plexitis in those with complicated, severe disease, suggest that this could represent a histopathologic marker of more aggressive disease. 

Retracted: No

PubPeer comments:
 Figure 4C - more similar than expected. Could authors check it please? ![file] ,