PReD-Bench/PRed-Bench huggingface dataset:
Roles of long noncoding RNAs in gastric cancer and their clinical applications
Authors: Junming Guo
Chunjing Xu
Weiliang Sun
Yunben Yang
Yi Xie
Journal: Journal of Cancer Research and Clinical Oncology (2016)
Discipline: CLINICAL MEDICINE
Keywords: Biological function; Clinical relevance; Gene expression; Long noncoding RNA; Regulatory mechanism
Affiliations: Ningbo Yinzhou People's Hospital and the Affiliated Yinzhou Hospital, Ningbo University School of Medicine, 315040, Ningbo, China., Zhejiang Key Laboratory of Pathophysiology, Department of Biochemistry and Molecular Biology, Ningbo University School of Medicine, 315211, Ningbo, China., Zhejiang Key Laboratory of Pathophysiology, Department of Biochemistry and Molecular Biology, Ningbo University School of Medicine, 315211, Ningbo, China. .

Abstract:  Purpose: Gastric cancer ranks as the most common cancer in the world. However, the progresses of its diagnosis and treatment are still not satisfactory. The purpose of this study is to summarize the roles of lncRNAs associated with gastric cancer. Methods: We searched lncRNAs associated with gastric cancer in PubMed. Results: Long noncoding RNAs (lncRNAs), transcripts larger than 200 nucleotides, regulate gene expression at various levels. They are playing important roles in the occurrence and development of gastric cancer. They are involved in signaling pathways, crosstalk with microRNAs, and affecting metastasis by regulating epithelial-to-mesenchymal transition. By acting as oncogenes or tumor suppressors, lncRNAs contribute to gastric cancer occurrence and development. Several lncRNAs including HOTAIR, HULC, LINC00152, MALAT2, H19, GHET1, and GACAT3 have been demonstrated having oncogene activities, while other lncRNAs including LEIGC, GAS5, and FER1L4 have been thought as tumor suppressors. Conclusions: Several lncRNAs from tissue, blood, and gastric juice have shown potential values in gastric cancer diagnosis or prognosis evaluation. 

Retracted: No

PubPeer comments:
 Due to the retraction of an original study, this review may need to be errata. 2020 retraction. https: www.nature.com articles s41417-020-0177-8 The Editor-in-Chief is retracting this article [1]. Concerns were raised that the MALAT2 gene described does not exist. This has been confirmed by post-publication peer review: there is only one transcript, which is called MALAT1. None of the authors has responded to correspondence from the Editor-in-Chief or the Publisher about this retraction. Reference 1. Chen F, Tian Y, Pang E, Wang Y, Li L. MALAT2-activated long noncoding RNA indicates a biomarker of poor prognosis in gastric cancer. Cancer Gene Ther. 2015; https: doi.org 10.1038 cgt.2015.6 ,
MicroRNA-148a suppresses epithelial-to-mesenchymal transition by targeting ROCK1 in non-small cell lung cancer cells
Authors: Yiping Wang
Jipeng Li
Yulan Song
Jianping Luo
Wanjun Yu
Journal: Molecular and Cellular Biochemistry (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: miRNAs; epithelial-to-mesenchymal transition (EMT); miR-148a; non-small cell lung cancer (NSCLC); lymph-node metastasis
Affiliations: Department of Clinical Laboratory, Yinzhou People's Hospital, Ningbo 315040, China.

Abstract:  Recent studies have implied that miRNAs act as crucial modulators for epithelial-to-mesenchymal transition (EMT). We found that miR-148a is significantly downregulated in non-small cell lung cancer (NSCLC) compared to adjacent non-cancerous lung tissues, and the downregulated miR-148a was significantly associated with lymph-node metastasis. Functional assays demonstrated that miR-148a inhibited EMT in NSCLC cells. Moreover, miR-148a decreased 3'-untranslated region luciferase activity of ROCK1 and ROCK1 protein expression. Knockdown of ROCK1 reversed EMT resembling that of miR-148a overexpression. Furthermore, ROCK1 was widely upregulated in NSCLC, and its mRNA levels were inversely correlated with miR-148a expression. These findings suggest that miR-148a acts as a novel EMT suppressor in NSCLC cells, at least in part by modulation of ROCK1. 

Retracted: No

PubPeer comments:
 Figure 4g. https: imgur.com VRgBIaS ,
Peroxisome proliferator-activated receptor β/δ induces myogenesis by modulating myostatin activity
Authors: Ravi Kambadur
Walter Wahli
Sudarsanareddy Lokireddy
Sabeera Bonala
Mridula Sharma
Harikumar Arigela
Craig McFarlane
Serena Teng
Journal: Journal of Biological Chemistry (2012)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: PPARβ/δ; myogenesis; Gasp-1; myoblast proliferation; differentiation
Affiliations: School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore.

Abstract:  Classically, peroxisome proliferator-activated receptor β/δ (PPARβ/δ) function was thought to be restricted to enhancing adipocyte differentiation and development of adipose-like cells from other lineages. However, recent studies have revealed a critical role for PPARβ/δ during skeletal muscle growth and regeneration. Although PPARβ/δ has been implicated in regulating myogenesis, little is presently known about the role and, for that matter, the mechanism(s) of action of PPARβ/δ in regulating postnatal myogenesis. Here we report for the first time, using a PPARβ/δ-specific ligand (L165041) and the PPARβ/δ-null mouse model, that PPARβ/δ enhances postnatal myogenesis through increasing both myoblast proliferation and differentiation. In addition, we have identified Gasp-1 (growth and differentiation factor-associated serum protein-1) as a novel downstream target of PPARβ/δ in skeletal muscle. In agreement, reduced Gasp-1 expression was detected in PPARβ/δ-null mice muscle tissue. We further report that a functional PPAR-responsive element within the 1.5-kb proximal Gasp-1 promoter region is critical for PPARβ/δ regulation of Gasp-1. Gasp-1 has been reported to bind to and inhibit the activity of myostatin; consistent with this, we found that enhanced secretion of Gasp-1, increased Gasp-1 myostatin interaction and significantly reduced myostatin activity upon L165041-mediated activation of PPARβ/δ. Moreover, we analyzed the ability of hGASP-1 to regulate myogenesis independently of PPARβ/δ activation. The results revealed that hGASP-1 protein treatment enhances myoblast proliferation and differentiation, whereas silencing of hGASP-1 results in defective myogenesis. Taken together these data revealed that PPARβ/δ is a positive regulator of skeletal muscle myogenesis, which functions through negatively modulating myostatin activity via a mechanism involving Gasp-1. 

Retracted: Yes

PubPeer comments:
null, 
 https: www.straitstimes.com singapore 3-spore-based-scientists-linked-to-research-fraud ,
Missense mutation of VKORC1 leads to medial arterial calcification in rats
Authors: Virginie Lattard
Leon J Schurgers
Etienne Benoit
Benjamin Matagrin
Jean-Valéry Debaux
Arnaud Michaux
Journal: Scientific Reports (2018)
Discipline: Multidisciplinary
Keywords: Vitamin K; vascular calcifications; matrix Gla protein; VKORC1; mutations
Affiliations: USC 1233 RS2GP, INRA, VetAgro Sup, Univ Lyon, F-69280, Marcy l'Etoile, France., Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands., USC 1233 RS2GP, INRA, VetAgro Sup, Univ Lyon, F-69280, Marcy l'Etoile, France. .

Abstract:  Vitamin K plays a crucial role in the regulation of vascular calcifications by allowing activation of matrix Gla protein. The dietary requirement for vitamin K is low because of an efficient recycling of vitamin K by vitamin K epoxide reductase (VKORC1). However, decreased VKORC1 activity may result in vascular calcification. More than 30 coding mutations of VKORC1 have been described. While these mutations have been suspected of causing anticoagulant resistance, their association with an increase in the risk of vascular calcification has never been considered. We thus investigated functional cardiovascular characteristics in a rat model mutated in VKORC1. This study revealed that limited intake in vitamin K in mutated rat induced massive calcified areas in the media of arteries of lung, aortic arch, kidneys and testis. Development of calcifications could be inhibited by vitamin K supplementation. In calcified areas, inactive Matrix Gla protein expression increased, while corresponding mRNA expression was not modified. Mutation in VKORC1 associated with a limited vitamin K intake is thus a major risk for cardiovascular disease. Our model is the first non-invasive rat model that shows spontaneous medial calcifications and would be useful for studying physiological function of vitamin K. 

Retracted: No

PubPeer comments:
 In Table 1, the values for body weight and uremia are exactly the same. Why? In addition, there are several cases where data values are identical accross different groups of rats. ![file] ,
Herpes simplex virus type 1 strain HSV1716 grown in baby hamster kidney cells has altered tropism for nonpermissive Chinese hamster ovary cells compared to HSV1716 grown in vero cells
Authors: Frazer J Rixon
S Moira Brown
Joe Conner
Journal: Journal of Virology (2005)
Discipline: MICROBIOLOGY
Keywords: Chinese hamster ovary cells; CHO cells; herpes simplex virus type 1; HSV-1; infection
Affiliations: Crusade Laboratories Ltd., Institute of Neurological Sciences, Southern General Hospital, 1345 Govan Rd., Glasgow G51 4TF, Scotland, United Kingdom, MRC Virology Unit, Institute of Virology, Church Street, Glasgow G11 5JR, Scotland, United Kingdom

Abstract:  Chinese hamster ovary (CHO) cells are traditionally regarded as nonpermissive cells for herpes simplex virus type 1 (HSV-1) infection as they lack the specific entry receptors, and modified CHO cells have been instrumental in the identification of HSV-1 receptors in numerous studies. In this report we demonstrate that the HSV-1 strain 17+ variant HSV1716 is able to infect unmodified CHO cells but only if the virus is propagated in baby hamster kidney (BHK) cells. Infection of CHO cells by BHK-propagated HSV1716 results in expression of immediate-early, early, and late viral genes, and infectious progeny virions are produced. In normally cultured CHO cells, up to a maximum of 50% of cells were permissive for BHK-propagated HSV1716 infection, with 24 h of serum starvation increasing this to 100% of CHO cells, suggesting that the mechanism used by BHK-propagated virus to infect CHO cells was cell cycle dependent. The altered tropism of HSV1716 was also evident in another nonpermissive mouse melanoma cell line and is an exclusive property resulting from propagation of the virus using BHK cells, as viruses propagated on Vero, C8161 (a human melanoma cell line), or indeed, CHO cells were completely unable to infect either CHO or mouse melanoma cells. 

Retracted: No

PubPeer comments:
 Figure 3a. Much more similar than expected. ![file] , 
 Figure 1. Much more similar than expected. ![file] ,
In-depth human plasma proteome analysis captures tissue proteins and transfer of protein variants across the placenta
Authors: Jochen M Schwenk
Albin Björk
Janne Lehtiö
Davide Tamburro
Marie Wahren-Herlenius
Maria Pernemalm
Hanna Åmark
Jorrit Boekel
Claes-Göran Östenson
Yafeng Zhu
AnnSofi Sandberg
Magnus Westgren
Journal: eLife (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: biomarker discovery; computational biology; human; human biology; mass spectrometry
Affiliations: Karolinska Institute, Stockholm, Sweden., Proteogenomics, Science for Life Laboratory, Sweden., Royal Institute of Technology, Stockholm, Sweden.

Abstract:  Here, we present a method for in-depth human plasma proteome analysis based on high-resolution isoelectric focusing HiRIEF LC-MS/MS, demonstrating high proteome coverage, reproducibility and the potential for liquid biopsy protein profiling. By integrating genomic sequence information to the MS-based plasma proteome analysis, we enable detection of single amino acid variants and for the first time demonstrate transfer of multiple protein variants between mother and fetus across the placenta. We further show that our method has the ability to detect both low abundance tissue-annotated proteins and phosphorylated proteins in plasma, as well as quantitate differences in plasma proteomes between the mother and the newborn as well as changes related to pregnancy. 

Retracted: No

PubPeer comments:
 In figure 4b, there are two different PSM counts for the protein FBN2 for third trimester after pregnancy , 
 Figure 4b shows two different values for the same protein (FBN2). Most likely a labeling error. ![file] ,
CircHIPK3 promotes colorectal cancer cells proliferation and metastasis via modulating of miR-1207-5p/FMNL2 signal
Authors: Meng Su
Baoli Qin
Yan Yan
Journal: Biochemical and Biophysical Research Communications (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Colorectal cancer; FMNL2; Proliferation/metastasis; circHIPK3; miR-1207-5p.
Affiliations: Department of Medical Oncology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, PR China. Electronic address: .

Abstract:  Increasing evidences demonstrate that circular RNAs (circRNAs) are extensively implicated in various cancers including colorectal cancer (CRC). In the present study, we found that circRNA HIPK3 (circPIK3) was upregulated in CRC. We identified that circHIPK3 was closely related with unfavorable clinicopathological features in patients with CRC. Functional transwell assay and proliferation assay indicated that circHIPK3 served as an oncogene and promoted CRC cells migration, invasion and proliferation. Meanwhile, we found that formin like 2 (FMNL2) was a key downstream molecule in circHIPK3-induced metastasis and proliferation in CRC cells. We further verified that circHIPK3 was mainly located at cytoplasm through an immunofluorescence assay. An online bioinformatics screening and a GEO datasets analysis showed that microRNA 1207-5p (miR-1207-5p) was downregulated in CRC. Also, we found that miR-1207-5p shared a similar miR-1207-5p response elements (MREs-1207-5p). Meanwhile, we showed that miR-1207-5p suppressed CRC cells migration, invasion and proliferation via directly targeting of FMNL2. Even further, via a constructed luciferase assay, we indicated that circHIPK3 was another target of miR-1207-5p. Functionally, we proved that circHIPK3 enhanced FMNL2 mediated promotion of migration, invasion and proliferation by sponging of miR-1207-5p in CRC cells. In summary, the outcomes of this study illustrated that circHIPK3 promoted CRC cells migration, invasion and proliferation modulating of FMNL2 by sponging of miR-1207-5p. Our findings indicated that circHIPK3/miR-1207-5p/FMNL2 axis might be a new strategy in molecular treatment of CRC. 

Retracted: No

PubPeer comments:
 The images in this paper have multiple areas of overlap, with some apparent editing. Common author on this paper: https: pubpeer.com publications ED88823E95B8CDD6F51E0809D0F510 and https: pubpeer.com publications ED88823E95B8CDD6F51E0809D0F510 *** ![file] ![file] ![file] ![file] ,
Undec-10-enoic acid functionalized chitosan based novel nano-conjugate: An enhanced anti-bacterial/biofilm and anti-cancer potential
Authors: Mohammad Owais
Khairujjaman Laskar
Abdul Rauf
Syed Mohd Faisal
Anees Ahmed
Journal: Carbohydrate Polymers (2017)
Discipline: CHEMISTRY
Keywords: Anti-bacterial; Anti-biofilm; Anti-cancer; Fatty acid; Nano-bioconjugate
Affiliations: Department of Chemistry, Aligarh Muslim University, Aligarh, 202002, India., Molecular Immunology Laboratory, Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh 202002, India., Department of Chemistry, Aligarh Muslim University, Aligarh, 202002, India. Electronic address: ., Hybridoma Laboratory, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.

Abstract:  Fatty acid functionalized chitosan conjugates are of great interest in cancer therapeutics because of its internalization through receptor mediated endocytosis into the cancer cells. Keeping the above fact into consideration, herein we synthesized the undec-10-enoic acid functionalized chitosan based undecyl-chitosan (U-CS) nano-bioconjugate with the use of DCC as a coupling agent. The U-CS conjugate synthesized was confirmed and characterized by FTIR, 1H NMR, TGA, XRD, SEM and TEM analysis. Generally, it is well established that conjugates of oleic acid with human Alpha-lactalbumin (HAMLET) induce cytotoxicity in the altered cells, but not in healthy cells. To check our presumptions, anti-bacterial and anti-cancer potential of U-CS was evaluated against bacterial pathogens (Gram +ve and Gram -ve) and human cancer cell lines (HeLa, MDA-MB-231 and Hep3B). The results of our study clearly revealed that conjugate showed enhance anti-bacterial, anti-biofilm as well as anti-cancer efficacy as compared to pure and free form of the chitosan. 

Retracted: No

PubPeer comments:
 Figure 4 shows zones of inhibitions of 5 different bacterial species (A through E) and 4 different concentrations of nano-bioconjugate. As such, one would expect 5*4 = 20 different images. Unexpectedly, this is not the case. Boxes of the same colors show panels that look unexpectedly similar, while arrows in that same color highlight their orientation. Could the authors please check? ![file] ,
The additive effect of aging on sepsis-induced cognitive impairment and neuroinflammation
Authors: Luana Cucker
João Quevedo
Rodrigo Olivieri
Diogo Dominguini
Mariane Abatti
Felipe Dal-Pizzol
Henrique Burger
Bruna Pescador
Monique Michels
Pricila Ávila
Journal: Journal of Neuroimmunology (2018)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Aging; Cognitive decline; Sepsis.
Affiliations: Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina, Criciúma, SC, Brazil., Laboratory of Neurosciences, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil., Laboratory of Neurosciences, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil; Translational Psychiatry Program, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA; Neuroscience Graduate Program, The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX, USA., Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina, Criciúma, SC, Brazil; Center of Excellence in Applied Neurosciences of Santa Catarina (NENASC), Graduate Program in Medical Sciences, Federal University of Santa Catarina (UFSC), Florianópolis, SC, Brazil. Electronic address: .

Abstract:  Systemic inflammation is emerging as a significant driver of cognitive decline in the aged and vulnerable brain. In sepsis survivors animals low-grade brain inflammation occurs, suggesting that sepsis is able to induce in microglia a primed-like state. The purpose of this study is to analyze the role of sepsis-induced brain inflammation in the progression of the physiological process of brain aging. Wistar rats 2month-old were subjected to sepsis and 60 and 90days after were submitted to the new object recognition test and brain was removed to the determination of cytokines, myeloperoxidase (MPO) activity, amyloid-beta peptide (Aβ) and immunohistochemistry markers of microglial activation. In the hippocampus, from 60 to 90days there was an increase in TNF-α and IL-1β levels in septic animals. This also occurred to the levels of IL-1β and IL-6 in the prefrontal cortex. This was associated with persistent increased in microglial activation and Aβ levels. In conclusion, neuroinflammation is persistent after sepsis and this could burst the usual inflammation that occurs during brain aging. 

Retracted: No

PubPeer comments:
 I have concerns about possible reused portions of bands in Figure 3A. *** ![file] ,
Activation of BAD by therapeutic inhibition of epidermal growth factor receptor and transactivation by insulin-like growth factor receptor
Authors: Nigel Bundred
Stanley J Korsmeyer
Ann M Ranger
Pengbo Wang
Anthony J Valentijn
Andrew P Gilmore
Michael J O&#x27;Hare
Alan Wakeling
Charles H Streuli
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: cancer chemotherapeutics; apoptosis; EGF receptor; ZD1839; pro-apoptotic protein
Affiliations: School of Biological Sciences, University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, United Kingdom. 

Abstract:  Novel cancer chemotherapeutics are required to induce apoptosis by activating pro-apoptotic proteins. Both epidermal growth factor (EGF) and insulin-like growth factor (IGF) provide potent survival stimuli in many epithelia, and activation of their receptors is commonly observed in solid human tumors. Here we demonstrate that blockade of the EGF receptor by a new drug in phase III clinical trails for cancer, ZD1839, potently induces apoptosis in mammary epithelial cell lines and primary cultures, as well as in a primary pleural effusion from a breast cancer patient. We identified the mechanism of apoptosis induction by ZD1839. We showed that it prevents cell survival by activating the pro-apoptotic protein BAD. Moreover, we demonstrate that IGF transactivates the EGF receptor and that ZD1839 blocks IGF-mediated phosphorylation of MAPK and BAD. Many cancer therapies kill tumor cells by inducing apoptosis as a consequence of targeting DNA; however, the threshold at which apoptosis can be triggered through DNA damage is often different from that in normal cells. Our results indicate that by targeting a growth factor-mediated survival signaling pathway, BAD phosphorylation can be manipulated therapeutically to induce apoptosis. 

Retracted: No

PubPeer comments:
 There are splicing traces (magenta arrowhead) in several immunoblot membranes. ![file] ,
Evodiamine Induces Apoptosis, G2/M Cell Cycle Arrest, and Inhibition of Cell Migration and Invasion in Human Osteosarcoma Cells via Raf/MEK/ERK Signalling Pathway
Authors: Jinlong Hu
Yuelai Zhou
Journal: Medical Science Monitor (2018)
Discipline: CLINICAL MEDICINE
Keywords: Osteosarcoma; Evodiamine; Anticancer activity; Apoptosis; Cell cycle analysis
Affiliations: Department of Orthopedic, College of Clinical Medicine, Yangzhou University, Northern Jiangsu People's Hospital, Yangzhou, Jiangsu, China (mainland)., Department of Orthopedics, Taizhou Fourth People's Hospital, Taizhou, Jiangsu, China (mainland).

Abstract:  BACKGROUND Osteosarcoma is a prevalent type of bone tumor mainly reported in children and adolescents. The treatments for osteosarcoma are limited and are associated with serious adverse effects. In this study we evaluated the anticancer activity of Evodiamine, a plant-derived natural product, against a panel of osteosarcoma cells and explored the underlying mechanisms. MATERIAL AND METHODS The viability of osteosarcoma cell lines was investigated by MTT assay. Apoptosis was detected by DAPI and annexin V/PI staining and cell cycle analysis was performed by flow cytometry. The expression of the proteins was examined by Western blotting. RESULTS The results of the present study indicated that Evodiamine inhibited the proliferation of U2OS osteosarcoma cells with an IC50 of 6 µM. Further investigations indicated the antiproliferative effects of Evodiamine are due to induction of apoptosis and G2/M cell cycle arrest. The results of Western blotting revealed that the expression of several apoptosis (Cytochrome c, Bax, Bid, Caspase 3, 9, 8, and PARP) and cell cycle-related proteins (cyclin B1, Cdc25c, and Cdc2) was significantly altered. Evodiamine also suppressed the migration and invasion of U2OS osteosarcoma cells. Moreover, Evodiamine downregulated the expression of important regulatory proteins such as p-MEK and p-ERK, leading to the inhibition of Raf/MEK/ERK signalling pathways. CONCLUSIONS We found that Evodiamine exerts anticancer effects on osteosarcoma cells and has potential in the treatment of osteosarcoma. 

Retracted: Yes

PubPeer comments:
 This article appears to be computer-generated with [SCIgen] . ![file] --- This comment was written by Guillaume Cabanac and Cyril Labbu00e9. Contact: [SeekAndBlastn-Operators@univ-grenoble-alpes.fr](mailto:SeekAndBlastn-Operators@univ-grenoble-alpes.fr). ,
Gene Expression Comparison Between the Primary Tumor and its Lymph Node Metastasis in Head and Neck Squamous Cell Carcinoma: A Pilot Study
Authors: Michel Peoc&#x27;h
Jean Marc Dumollard
Marie Gavid
Georgia Karpathiou
Marios Froudarakis
Jean Michel Prades
Marie-Laurie Stachowitz
Journal: Cancer Genomics & Proteomics (2019)
Discipline: CLINICAL MEDICINE
Keywords: Claudin; egfr; hpv; maspin; p16
Affiliations: Department of Pathology, North Hospital, University Hospital of St-Etienne, Saint-Étienne, France ., Department of Pathology, North Hospital, University Hospital of St-Etienne, Saint-Étienne, France., Department of Head and Neck Surgery, North Hospital, University Hospital of St-Etienne, Saint-Étienne, France., Department of Pneumonology, North Hospital, University Hospital of St-Etienne, Saint-Étienne, France.

Abstract:  Background/aim: In metastatic head and neck squamous cell carcinoma (HNSCC) the metastatic tumor does not always keep the same gene expression profile as the parental tumor, which may influence the course of the disease. The aim of this study was to compare the expression of genes implicated in HNSCC carcinogenesis between the primary tumor and the corresponding lymph node metastasis. Materials and methods: Eighteen HNSCC, their corresponding node metastases and non-neoplastic tissues were studied by RT-qPCR for the expression of EGFR, VEGF, claudin7, maspin, survivin and SCCA. The levels of expression were correlated with histological characteristics and patients' prognosis. Results: All genes except for survivin displayed different expression in node metastasis compared to the primary tumor. The expression of EGFR, survivin, maspin, and claudin7 in node metastasis and SSCA in the primary tumor affected the prognosis. SCCA expression is associated with the expression of claudin7 and maspin. P16-positive tumors expressed low levels of VEGF and SCCA, while keratinizing tumors over-expressed VEGF. Conclusion: Differential gene expression levels in node metastases compared to the primary tumor is linked to the prognosis of HNSCC patients. The histological/immunohisto-chemical characteristics of the tumor are associated with these genes expression changes. 

Retracted: No

PubPeer comments:
 The results are not the same as those obtained from other larger databases , see : https: www.nature.com articles nature14129 ,
LncRNA XIST promotes the progression of laryngeal squamous cell carcinoma via sponging miR-125b-5p to modulate TRIB2
Authors: Ping Guo
Shenfa Zhuang
Chunxiu Liu
Zhenjun Lu
Hui Liu
Journal: Bioscience Reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LncRNA XIST; TRIB2; laryngeal squamous cell carcinoma; miR-125b-5p.
Affiliations: Department of Otolaryngology, Jining First People's Hospital of Shandong Province, Jining, Shandong, China., Department of Otolaryngology, The Third People's Hospital, Qingdao, Shandong, China.

Abstract:  Objective: X inactivate-specific transcript (XIST) is an attractive long noncoding RNA (lncRNA) functioning as an indicator of various human tumors, including laryngeal squamous cell carcinoma (LSCC). The present study was conducted to explore a novel regulatory network of lncRNA XIST in LSCC cells. Materials and methods: Quantitative real-time polymerase chain reaction (QRT-PCR) was used to detect the expression levels of XIST, miR-125b-5p and TRIB2 in LSCC cells and tissues. Cell proliferation, apoptosis, migration and invasion were detected by Cell Counting Kit-8 (CCK-8), flow cytometry and Transwell assays, separately. The relationship among XIST, miR-125b-5p and tribbles homolog 2 (TRIB2) was predicted by starBase v2.0 or TargetScan and confirmed by Dual-luciferase reporter assay. The TRIB2 protein expression was quantified by Western blot assay. Murine xenograft model was utilized to validate the role of XIST in vivo. Results: XIST was notably up-regulated in LSCC tissues and cells, and the high level of XIST was associated with the low survival rate of LSCC patients. XIST knockdown markedly repressed cell proliferation, migration and invasion and promoted the apoptosis of LSCC cells and the effects were antagonized by loss of miR-125b-5p. MiR-125b-5p was a target of XIST in LSCC cells, and it could bind to TRIB2 as well. Moreover, XIST-loss-induced down-regulation of TRIB2 could be significantly reversed by miR-125b-5p knockdown. XIST promoted the growth of LSCC tumor in vivo. Conclusion: LncRNA XIST promoted the malignance of LSCC cells partly through competitively binding to miR-125b-5p, which in turn increased TRIB2 expression. 

Retracted: Yes

PubPeer comments:
 Retracted [11 January 2022] . ----------------------------------- This article is being retracted from Bioscience Reports at the request of the authors, as the results of the repeated experiments did not show the statistical differences seen in the original study. Hence, the authors of this study feel the results of this paper are unreliable. The Editor-in-Chief and Editorial Board agree with the Retraction. ---------------------------------------------- The Western Blots and flow-cytometry apoptosis scatterplots fall into familiar styles. Figure 2 E F: ![file] For comparison: Fig 2C of [Gong Zhu (2020)] **[retracted for papermill origins]**. ![] Fig 2G of [Jiang et al (2020)] **[retracted on authors request]** ![] ,
Pharmacological inhibition of DNA methylation induces proinvasive and prometastatic genes in vitro and in vivo
Authors: Alexander Unterberger
Moshe Szyf
Shafaat A Rabbani
Bushra Ateeq
Journal: Neoplasia (2008)
Discipline: CLINICAL MEDICINE
Keywords: DNA methylation inhibitor; 5-aza-2'-deoxycytidine; demethylation; tumor suppressor genes; invasion
Affiliations: Department of Medicine, McGill University, Montreal, Quebec, Canada.

Abstract:  The mechanism of action of DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-CdR), a potential anticancer agent is believed to be activated by the demethylation of tumor suppressor genes. We tested here the hypothesis that demethylating agents also demethylate and activate genes involved in invasion and metastasis and therefore might increase the risk of developing tumor metastasis. The effect of 5-aza-CdR on noninvasive human breast cancer cells MCF-7 and ZR-75-1 was evaluated by cell proliferation, invasion, and migration assay. The ability of 5-aza-CdR to activate a panel of silenced prometastatic and tumor suppressor genes was evaluated using reverse transcription-polymerase chain reaction and bisulfite DNA sequence analysis in vitro and for change in tumor growth and gene expression in vivo. Treatment of MCF-7 and ZR-75-1 with 5-aza-CdR diminished cell proliferation, induced tumor suppressor RASSF1A, and altered cell cycle kinetics' G(2)/M-phase cell cycle arrest. While these effects of 5-aza-CdR slowed the growth of tumors in nude mice, it also induced a battery of prometastatic genes, namely, uPA, CXCR4, HEPARANASE, SYNUCLEIN gamma, and transforming growth factor-beta (TGF-beta), by demethylation of their promoters. These results draw attention to the critical role of demethylation as a potential mechanism that can promote the development and progression of tumor metastasis after demethylation therapy as an anticancer treatment. 

Retracted: No

PubPeer comments:
 Figure 1E. Much more similar than expected. ![file] , 
 Figure 1E. Much more similar and different than expected. ![file] ,
A highly X-ray sensitive iridium prodrug for visualized tumor radiochemotherapy
Authors: Zhennan Zhao
Pan Gao
Tianfeng Chen
Li Ma
Journal: Chemical Science (2020)
Discipline: CHEMISTRY
Keywords: radiotherapy; chemotherapy; tumor targeting therapy; Ir-based prodrug; sensitization efficiency
Affiliations: Department of Chemistry, Jinan University, Guangzhou 510632, China

Abstract:  Concomitant treatment of radiotherapy and chemotherapy is widely used in cancer therapy. The search for highly efficient radiochemotherapy drugs for tumor targeting therapy under image-guiding is of considerable interest. Herein we report an Ir-based prodrug Ir-NB with high sensitization efficiency for in vivo tumor microenvironment responsive cancer-targeted bioimaging radiochemotherapy. To the best of our knowledge, the sensitivity enhancement ratio (SER) of the Ir-NB prodrug is the highest among those reported for radiotherapy metal complex drugs. From detailed action mechanism study, we provide evidence that the prodrug is effectively suppresses the tumor growth through inducing mitochondrial dysfunction, and eventually amplifies the apoptotic signal pathway. This study provides an approach for the development of cancer theranostic agents for tumor radiotherapy. 

Retracted: No

PubPeer comments:
 Note: This article has been corrected. Please see the link below: https: www.oncotarget.com article 17684 ,
Downregulation of hsa_circ_0001836 Induces Pyroptosis Cell Death in Glioma Cells via Epigenetically Upregulating NLRP1
Authors: Qiang Meng
Hao Wu
Shan Dong
Huanfa Li
Yong Liu
Jiangpeng Jing
Journal: Frontiers in Oncology (2021)
Discipline: CLINICAL MEDICINE
Keywords: NLRP1; circular RNA; glioma; methylation; pyroptosis.
Affiliations: Department of Neurosurgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Abstract:  Background: It has been shown that circular RNAs (circRNAs) play a vital role in the progression of glioma. Recently, hsa_circ_0001836 was found to be upregulated in glioma tissues, but the role of hsa_circ_0001836 in glioma remains unclear. Methods: EdU staining and flow cytometry assays were used to measure the viability and death of glioma cells. In addition, scanning electron microscopy (SEM) was used to observe the morphology of cells undergoing cell death. Results: Hsa_circ_0001836 expression was upregulated in U251MG and SHG-44 cells. In addition, hsa_circ_0001836 knockdown significantly reduced the viability and proliferation of U251MG and SHG-44 cells. Moreover, hsa_circ_0001836 knockdown markedly induced the pyroptosis of U251MG and SHG-44 cells, evidenced by the increased expressions of NLRP1, cleaved caspase 1 and GSDMD-N. Meanwhile, methylation specific PCR (MSP) results indicated that hsa_circ_0001836 knockdown epigenetically increased NLRP1 expression via mediating DNA demethylation of NLRP1 promoter region. Furthermore, downregulation of hsa_circ_0001836 notably induced pyroptosis and inhibited tumor growth in a mouse xenograft model of glioma. Conclusion: Collectively, hsa_circ_0001836 knockdown could induce pyroptosis cell death in glioma cells in vitro and in vivo via epigenetically upregulating NLRP1 expression. These findings suggested that hsa_circ_0001836 may serve as a potential therapeutic target for the treatment of glioma. 

Retracted: Yes

PubPeer comments:
 Retracted [29 December 2021] . H t [RetractionWatch] . ----------------------- The journal and Chief Editors retract the 31 March 2021 article cited above. Following publication, concerns were raised regarding the validity of the data in the article. The authors failed to provide the raw data or a satisfactory explanation during the investigation, which was conducted in accordance with Frontiersu2019 policies. Given the concerns, and the lack of raw data, the editors no longer have confidence in the findings presented in the article. This retraction was approved by the Chief Editors of Frontiers in Oncology and the Chief Executive Editor of Frontiers. The authors have not responded to any correspondence regarding the retraction. ------------------------------ It would helpful to learn more about these concerns that were raised , and who raised them. ,
Distinct functional domains of Nbs1 modulate the timing and magnitude of ATM activation after low doses of ionizing radiation
Authors: Jiri Lukas
Jacob Falck
Zuzana Horejsí
Jiri Bartek
Michael B Kastan
Christopher J Bakkenist
Journal: Oncogene (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: ATM kinase; tumour suppressor; genome integrity checkpoints; ionizing radiation; DNA double-strand breaks
Affiliations: Danish Cancer Society, Institute of Cancer Biology, Strandboulevarden 49, Copenhagen DK-2100 Denmark.

Abstract:  The ATM kinase is a tumour suppressor and a key activator of genome integrity checkpoints in mammalian cells exposed to ionizing radiation (IR) and other insults that elicit DNA double-strand breaks (DSBs). In response to IR, autophosphorylation on serine 1981 causes dissociation of ATM dimers and initiates cellular ATM kinase activity. Here, we show that the kinetics and magnitude of ATM Ser1981 phosphorylation after exposure of human fibroblasts to low doses (2 Gy) of IR are altered in cells deficient in Nbs1, a substrate of ATM and a component of the MRN (Mre11-Rad50-Nbs1) complex involved in processing/repair of DSBs and ATM-dependent cell cycle checkpoints. Timely phosphorylation of both ATM Ser1981 and the ATM substrate Smc1 after IR were rescued via retrovirally mediated reconstitution of Nbs1-deficient cells by wild-type Nbs1 or mutants of Nbs1 defective in the FHA domain or nonphosphorylatable by ATM, but not by Nbs1 lacking the Mre11-interaction domain. Our data indicate that apart from its role downstream of ATM in the DNA damage checkpoint network, the MRN complex serves also as a modulator/amplifier of ATM activity. Although not absolutely required for ATM activation, the MRN nuclease complex may help reach the threshold activity of ATM necessary for optimal genome maintenance and prevention of cancer. 

Retracted: No

PubPeer comments:
 2b. Mcm7 panel. Band lane 2, after vertical stretching, is very similar to band lane 5. ![file] , 
 #1 Not a convincing match, to my eyes. , 
 #2 I accept partial responsibility. I studied this for a while. Original scans would help. ,
Aluminum-Induced Synaptic Plasticity Impairment via PI3K-Akt-mTOR Signaling Pathway
Authors: Baolong Pan
Yaqin Li
Yanhong Wang
Tao Huang
Yanni Wang
Liang Li
Huaxing Meng
Xingli Xue
Qiao Niu
Huan Li
Journal: Neurotoxicity research (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Aluminum; Mammalian target of rapamycin (mTOR); Phosphatidylinositol 3-kinase (PI3K); Protein kinase B (Akt); Synaptic plasticity.
Affiliations: Department of Occupational Health, School of Public Health, Shanxi Medical University, Xinjian south Road, Taiyuan, Shanxi, People's Republic of China., Key Lab of Environmental Hazard and Health of Shanxi Province, Shanxi Medical University, Taiyuan, China., Key Lab of Cellular Physiology of Education Ministry, Shanxi Medical University, Taiyuan, China., Department of Occupational Health, School of Public Health, Shanxi Medical University, Xinjian south Road, Taiyuan, Shanxi, People's Republic of China. ., Key Lab of Environmental Hazard and Health of Shanxi Province, Shanxi Medical University, Taiyuan, China. ., Key Lab of Cellular Physiology of Education Ministry, Shanxi Medical University, Taiyuan, China. .

Abstract:  Aluminum (Al) is an environmental neurotoxin with extensive exposure by humans, but the molecular mechanism of its toxicity is still unclear. Several studies have indicated that exposure to aluminum can impair learning and memory function. The purpose of this study was to investigate the mechanism of LTP injury and the effect of aluminum exposure on related signal pathways. The results showed that the axonal dendrites of neurons in the hippocampal CA1 area of rats exposed to maltol aluminum showed neuritic beading and the dendritic spines were reduced. This resulted in dose-dependent LTP inhibition and led to impaired learning and memory function in rats. The PI3K-Akt-mTOR pathway may play a crucial role in this process. 

Retracted: No

PubPeer comments:
 Figure5A and Figure5C ![file] , 
 Figure5A and Figure5C ![file] , 
 #1 This figure is not ours. , 
 #3 Forestiera Eggersiana seems to have intended comment #1 for another thread . If that is the case, the present authors deserve an apology. Also, apologies from me to everyone for telling other contributors what to do. , 
 #2 Thank you very much for your careful reading of our pulication. I give an explanation as for the image of internal reference GAPDH in this part of the Figures(Fig.5 a Fig.5 c.) . At first, we had put the proteins and phosphorylated proteins in a single figure, there is only one inner reference GAPDH strip in a figure, we used the inner reference GAPDH strip in the figure, but the figure seemed too large and complicated. In order to describe the expression of proteins in more detailly and clearly, we divided the figure into two figures and described the bands of proteins and phosphorylated proteins respectively. In two figures, we used the same inner reference GAPDH strip, and this is acceptable, because it is a inner reference GAPDH strip. However, if it is necessary, we can choose a new inner reference GAPDH strip chart from our orininal data. ,
LASP1-S100A11 axis promotes colorectal cancer aggressiveness by modulating TGFβ/Smad signaling
Authors: Yuhao Luo
Ya Niu
Yanqing Ding
Lijun Xu
Feifei Zhang
Liang Zhao
Jiaqi Yang
Ziyun Shao
Hui Wang
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: LASP1; S100A11; CRC progression; metastasis; TGFβ
Affiliations: Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China., Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China., Department of Medical Oncology, Affiliated Tumor Hospital of Guangzhou Medical University, Guangzhou, China.

Abstract:  LIM and SH3 protein 1(LASP1) can promote colorectal cancer (CRC) progression and metastasis, but the mechanism remains unclear. Here, we show that LASP1 interacts with S100 calcium binding protein A11(S100A11) and enhances its expression in CRC. LASP1-S100A11 axis is essential for TGFβ-mediated epithelial-mesenchymal transition (EMT) and cell aggressive phenotype. Clinically, S100A11 is overexpressed in CRC tissues and localized in both the cytoplasm and the nucleus of CRC cells. Overexpression of S100A11 in cytoplasmic and nuclear subcellular compartments is associated with tumor metastasis and poor prognosis of CRC patients. Introduction of cytoplasmic and nuclear S100A11 promotes aggressive phenotypes of CRC cells in vitro as well as growth and metastasis of CRC xenografts, whereas suppressing S100A11 abrogates these effects. Furthermore, we identify flotillin-1 (FLOT1) and histone H1 as downstream factors for cytoplasmic and nuclear pathway of S100A11, which are required for LASP1-S100A11 axis-mediated EMT and CRC progression. These findings indicate S100A11, combined with LASP1, plays a critical role in promoting CRC metastasis via its subcellular effectors, FLOT1 and histone H1. 

Retracted: No

PubPeer comments:
 Fig. 6D and Fig. 6E. Images were reused. ![file] , 
 Fig. 4B and Fig. 4E. After horizontal flipping of one WB band, two WB bands shown in red boxes appear more similar than expected. ![file] ,
The alpha subunit of the granulocyte-macrophage colony-stimulating factor receptor interacts with c-Kit and inhibits c-Kit signaling
Authors: Juan M Cárcamo
David W Golde
Jian Chen
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: GM-CSF; GMR; c-Kit; cytokine receptors; signal transduction
Affiliations: Department of Pharmacology, Weill Graduate School of Medical Sciences of Cornell University, New York, New York 10021, USA.

Abstract:  The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) regulates hematopoiesis and the function of mature host defense cells through the GM-CSF receptor (GMR), which is composed of alpha (alphaGMR) and beta (betaGMR) subunits. Stem cell factor is another important hematopoietic cytokine that signals through c-Kit, a receptor tyrosine kinase, and regulates hematopoietic stem cell maintenance and erythroid development. Like other cytokine receptors, GMR and c-Kit are generally deemed as independent adaptor molecules capable of transducing cytokine-specific signals. We found that the alphaGMR directly interacts with c-Kit and that the interaction is mediated by the cytoplasmic domains. Furthermore, alphaGMR inhibited c-Kit auto-phosphorylation induced by the ligand stem cell factor. Consistent with the inhibitory effect, the expression of alphaGMR was suppressed in cells whose viability was dependent on c-Kit signaling. In contrast, the alternatively spliced alpha2 isoform of the alphaGMR could not inhibit c-Kit signaling, providing a rationale for the existence of the alpha2 isoform. Our results suggest that in addition to having the commonly appreciated roles in cytokine signal transduction, the receptors alphaGMR and c-Kit could interact to coordinate their signal initiation. 

Retracted: No

PubPeer comments:
 It is hard to believe that the findings reported in this study, if true, have any physiological meaning. Even if u00abloci implicated in the central control of appetiteu00bb were differentially methylated in the sperm of obese men compared with controls, what is the status of those loci in the oocyte and in the embryo after fertilization? DNA methylation is highly developmentally regulated and tissue-specific, how do findings in sperm correlate with the situation in the embryo and, later, in the child and in the adult ? ,
Expression of three proteins in endometrioid adenocarcinoma and their significance in clinical nursing, diagnosis and treatment
Authors: Y Cui
X-Y Yin
S-M Zhang
X Yang
Journal: European review for medical and pharmacological sciences (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: NEDD9; BCAR1/P130CAS; paxillin; endometrioid adenocarcinoma; prognosis
Affiliations: Department of Gynecology, Affiliated Hongqi Hospital of Mudanjiang Medical University, Mudan Jiang City, Heilongjiang Province, China. .

Abstract:  Objective: This study aimed to investigate the role of NEDD9 (neural precursor cell expressed developmentally down-regulated 9), BCAR1/P130CAS (BCAR1/P130 Crk-associated substrate) and paxillin in predicting the prognosis of endometrioid adenocarcinoma (EA), so as to guild the nursing of EA. Patients and methods: A total of 65 patients who visited Affiliated Hongqi Hospital of Mudanjiang Medical University between June 2015 and June 2017 were enrolled. They underwent gynecological surgery and had their EA confirmed by pathology, and they were assigned to the EA group. All EA tissues were sampled and archived in paraffin blocks. In addition, 40 specimens of atypical endometrial hyperplasia (EAH) (the EAH group) and 40 specimens of normal proliferative endometria with benign uterine fibroids (the EN group) were selected as controls. The protein levels of NEDD9, BCAR1/P130CAS, and paxillin in each group were then detected by immunohistochemical staining. Results: The expression of the three proteins in the EA group and EAH group was significantly higher than that in the EN group, and their expression was significantly correlated with the clinical stage, histological grade and lymph node metastasis of EA. In addition, the expression of NEDD9, BCAR1/P130CAS, and paxillin in the EA group was positively correlated with each other. Conclusions: BCAR1/P130CAS and paxillin interact with NEDD9 to participate in the growth and migration of EA cells. Therefore, their proteins can be used as biomarkers for the diagnosis, treatment, and prognosis of EA. 

Retracted: No

PubPeer comments:
  Figure 1. Distribution of three proteins in tissues (A, paxillin; B, BCAR1 P130CAS; C, NEDD9; 1, endometrial adenocarcinoma; 2, endometrial atypical hyperplasia; 3, normal endometrial tissue) . Panels A3 and B3 appear to overlap (apart from a 12-deg rotation), with any differences between them being localised to small sections of the image. ![file] B2 and C2 also appear to overlap, with only localised differences. ![file] , 
 Closer attention reveals repeated elements within A2 and B3. I did not seek further. ![file] ![file] , 
 Whoops, missed another overlap. ![file] ,