PReD-Bench/PRed-Bench huggingface dataset:
Oral administration of recombinant adeno-associated virus elicits human immunodeficiency virus-specific immune responses
Authors: Kumiko Hashimoto
Kenji Hamajima
Yasuko Kumamoto
Kenji Okuda
Dennis Klinman
Yoshitsugu Kojima
Ke-Qin Xin
Nao Jounai
Shin Sasaki
Koji Okudela
Takaaki Ooki
Keiya Ozawa
Hiroaki Mizukami
Journal: Human Gene Therapy (2002)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Oral vaccines; mucosal immunity; regional cell-mediated immunity; infectious diseases; acquired immunodeficiency syndrome
Affiliations: Department of Bacteriology, Yokohama City University School of Medicine, Yokohama 236-0004, Japan, Division of Genetic Therapeutics, Center for Molecular Medicine, Jichi Medical School, Tochigi-ken 329-0498, Japan, Department of Pathology, Yokohama City University School of Medicine, Yokohama 236-0004, Japan, Department of Bioregulation, Leprosy Research Center, National Institute of Infectious Diseases, Tokyo 189-0002, Japan, Center for Biologics Evaluation and Research, U.S. Food and Drug Administration, Bethesda, MD 20892

Abstract:  Oral vaccines can induce both systemic and mucosal immunity. Mucosal immunity, especially regional cell-mediated immunity, plays an important role in protecting individuals from infectious diseases such as acquired immunodeficiency syndrome. In this study, a recombinant adeno-associated virus vector expressing human immunodeficiency virus type 1 env gene (AAV-HIV) was orally administered to BALB/c mice. Systemic and regional immunity was induced in the mice. Furthermore, the immunization significantly reduced viral load after an intrarectal challenge with a recombinant vaccinia virus expressing HIV env gene. Moreover, we also show that dendritic cells might contribute to the AAV-HIV vector-induced immune responses. 

Retracted: No

PubPeer comments:
 Figure 5. * Red boxes: The two AAV-LacZ panels look more similar than expected. The top panel has two extra Tetris blocks. ![file] ,
To eat or not to eat? Kinematics and muscle activity of reach-to-grasp movements are influenced by the action goal, but observers do not detect these differences
Authors: Carmel Houston-Price
Arran T Reader
Katherine R Naish
Andrew J Bremner
Nicholas P Holmes
Journal: Experimental brain research (2013)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: mirror neuron system; predictive ability; early differences; actions; goals
Affiliations: School of Psychology and Clinical Language Sciences, University of Reading, Earley Gate, Whiteknights, Reading, RG6 6AL, UK. 

Abstract:  Recent evidence suggests that the mirror neuron system responds to the goals of actions, even when the end of the movement is hidden from view. To investigate whether this predictive ability might be based on the detection of early differences between actions with different outcomes, we used electromyography (EMG) and motion tracking to assess whether two actions with different goals (grasp to eat and grasp to place) differed from each other in their initial reaching phases. In a second experiment, we then tested whether observers could detect early differences and predict the outcome of these movements, based on seeing only part of the actions. Experiment 1 revealed early kinematic differences between the two movements, with grasp-to-eat movements characterised by an earlier peak acceleration, and different grasp position, compared to grasp-to-place movements. There were also significant differences in forearm muscle activity in the reaching phase of the two actions. The behavioural data arising from Experiments 2a and 2b indicated that observers are not able to predict whether an object is going to be brought to the mouth or placed until after the grasp has been completed. This suggests that the early kinematic differences are either not visible to observers, or that they are not used to predict the end-goals of actions. These data are discussed in the context of the mirror neuron system. 

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: The problem in Experiment 2 is that we can t be sure there was any *signal* for observers to detect - we know that people couldn t detect it, but maybe it wasn t there in the first place? Better studies were done on this topic later, by others. ,
Macrophage migration inhibitory factor promotes the invasion and metastasis of oral squamous cell carcinoma through matrix metalloprotein‐2/9
Authors: Min Zheng
Ya-Ling Tang
Sha-Sha Wang
Xiang-Hua Yu
Mei Zhang
Xin Pang
Jia-Shun Wu
Jing-Biao Wu
Ya-Jie Tang
Xiao Yang
Xin-Hua Liang
Xiao-Lei Gao
Journal: Molecular Carcinogenesis (2019)
Discipline: CLINICAL MEDICINE
Keywords: epithelial-mesenchymal transition; invasion; macrophage migration inhibitory factor; metastasis; oral squamous cell carcinoma.
Affiliations: State Key Laboratory of Oral Diseases, Department of Oral and Maxillofacial Surgery, National Clinical Research Center for Oral DiseasesWest China Hospital of Stomatology Sichuan University Chengdu Sichuan China, Department of Stomatolog, Zhoushan HospitalWenzhou Medical University Zhoushan Zhejiang China, State Key Laboratory of Microbial TechnologyShandong University Qingdao China, Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei Key Laboratory of Industrial Microbiology, Hubei Provincial Cooperative Innovation Center of Industrial FermentationHubei University of Technology Wuhan China, State Key Laboratory of Oral Diseases, Department of Oral Pathology, National Clinical Research Center for Oral DiseasesWest China Hospital of Stomatology Sichuan University Chengdu Sichuan China

Abstract:  Macrophage migration inhibitory factor (MIF) has been shown to closely associate with the malignant progression of a variety of human carcinomas. However, the role and its underlying molecular mechanisms of MIF in the invasion and metastasis of oral squamous cell carcinoma (OSCC) still remains unclear. Here, we found that MIF silencing reduced the cell proliferation, migration, and invasion, as well as matrix metalloprotein-2 (MMP-2) and MMP-9 in OSCC cells. Overexpression of MMP-2 or MMP-9 restored the migration and invasion of MIF-knockdown cells, indicating that MMP-2 and MMP-9 are downstream targets of MIF. In the xenograft model, MIF silencing inhibited tumor growth and in lymph metastasis model, MIF silencing reduced tumor metastasis. More importantly, immunohistochemistry staining in a tissue microarray (TMA) demonstrated that MIF expression was positively correlated with clinic stage, recurrence, metastasis, and poor prognosis of patients with OSCC as well as with the levels of MMP-2 or MMP-9 in TMA. Therefore, our findings suggest that MIF may promote the invasion and metastasis of OSCC through the activation of MMP-2 and MMP-9 and prompt further investigation into the therapeutic value of MIF for OSCC treatment. 

Retracted: No

PubPeer comments:
 Figure 2B appears to show some image overlap. However, please note that the coloring has been altered and images flipped, suggesting that this is not simply an error during figure preparation. *** ![file] , 
 There also appears to be overlap between 2B and 4B. Again, difficult to believe these types of errors could occur by accident, and even if they did, it is hard to have confidence in this paperu2019s conclusions. *** 2B ![file] *** 4B ![file] , 
 ![file] ,
Retinoic acid and dexamethasone induce differentiation and maturation of somatotroph cells at different stages in vitro
Authors: Wenzhi Jia
Wenming Lv
Guanghui Zhang
Youzhi Lin
Yu Cheng
Qinghai Zhao
Songbin Fu
Shan Mi
Ying Xiang
Journal: Endocrine journal (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: retinoic acid; dexamethasone; growth hormone releasing hormone; somatotroph cell differentiation; embryonic pituitary gland
Affiliations: The Department of Neurological Surgery, First Affiliated Hospital, Harbin Medical University, Harbin, P.R.China.

Abstract:  The purpose of this study was to investigate the role of retinoic acid (RA) and/or dexamethasone and growth hormone releasing hormone (GHRH) in the induction of somatotroph cell differentiation. Immunohistochemistry, radioimmunoassay, 3-(4,5-dimethylthiazol -1,2-y1)-2,5-diphenyltetrazolium bromide assay, and immune electron microscopy were employed to determine the effect of incubation with these constituents on the differentiation into somatotrophs of cells isolated from the rat embryonic pituitary gland. RA administration increased the proportion of growth hormone (GH) positive somatotroph cells and GH secretion in embryonic pituitary cells (P&lt;0.01). After 4 days of incubation with RA, additional administration of dexamethasone further increased the proportion of somatotroph cells and GH secretion (P&lt;0.01), and increased the number of secretory granules in the somatotroph cells. Addition of GHRH alone had no such effect (P&gt;0.05). However, addition of GHRH to treatment with RA plus dexamethasone significantly increased both the proportion of somatotroph cells and the secretion of GH compared to treatment with RA or dexamethasone alone or RA plus dexamethasone (P&lt;0.01). RA promoted the early differentiation of somatotroph cells, dexamethasone promoted the differentiation and maturation of somatotroph cells and in addition, RA, dexamethasone and GHRH together exerted synergistic effects that markedly promoted somatotroph cell differentiation, maturation and GH secretion. 

Retracted: No

PubPeer comments:
 In Figure 1, a micrograph has been duplicated and presented as something else (different treatment). ![file] ,
Critical roles of mucin-1 in sensitivity of lung cancer cells to tumor necrosis factor-alpha and dexamethasone
Authors: Menglin Xu
Xiangdong Wang
Journal: Cell Biology and Toxicology (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Dexamethasone; Lung cancer; Mucin-1; Therapeutics; Tumor necrosis factor-alpha.
Affiliations: Department of Respiratory Medicine, The First Hospital of Wenzhou Medical University, Wenzhou, China., Department of Respiratory Medicine, The First Hospital of Wenzhou Medical University, Wenzhou, China. .

Abstract:  Lung cancer is the leading cause of death from cancer. Mucins are glycoproteins with high molecular weight, responsible for cell growth, differentiation, and signaling, and were proposed to be correlated with gene heterogeneity of lung cancer. Here, we report aberrant expression of mucin genes and tumor necrosis factor receptors in lung adenocarcinoma tissues compared with normal tissues in GEO datasets. Mucin-1 (MUC1) gene was selected and considered as the target gene; furthermore, the expression pattern of adenocarcinomic cells (A549, H1650, or H1299 cells) was validated under the stimulation with tumor necrosis factor-alpha (TNFα) or dexamethasone (DEX), separately. MUC1 gene interference was done to A549 cells to show its role in sensitivity of lung cancer cells to TNFα and DEX. Results of our experiments indicate that MUC1 may regulate the influence of inflammatory mediators in effects of glucocorticoids (GCs), as a regulatory target to improve therapeutics. It shows the potential effect of MUC1 and GCs in lung adenocarcinoma (LADC), which may help in LADC treatment in the future. 

Retracted: No

PubPeer comments:
 Fig 3D, 2 pairs of overlaps ![file] , 
 Also in Fig. 3, images of wound healing assay in plot C were missing all the details of the assay images. Can the authors please post the original images? ![file] Similar concern for Fig. 4D, although I m not posting the image here ,
TGF-beta directly targets cytotoxic T cell functions during tumor evasion of immune surveillance
Authors: Joan Massagué
Dori A Thomas
Journal: Cancer Cell (2005)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Tumors; immune surveillance; TGF-beta; cytotoxic T lymphocytes; CTLs
Affiliations: Cancer Biology and Genetics Program and Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.

Abstract:  Tumors escape from immune surveillance by producing the immunosuppressive cytokine TGF-beta. However, the mechanism by which TGF-beta inhibits T cell-mediated tumor clearance in vivo is unknown. We demonstrate that TGF-beta acts on cytotoxic T lymphocytes (CTLs) to specifically inhibit the expression of five cytolytic gene products-namely, perforin, granzyme A, granzyme B, Fas ligand, and interferon gamma-which are collectively responsible for CTL-mediated tumor cytotoxicity. Repression of granzyme B and interferon-gamma involves binding of TGF-beta-activated Smad and ATF1 transcription factors to their promoter regions, indicating direct and selective regulation by the TGF-beta/Smad pathway. Neutralization of systemic TGF-beta in mice enables tumor clearance with restoration of cytotoxic gene expression in antigen-specific CTLs in vivo. We suggest that TGF-beta suppresses CTL function in vivo through an anticytotoxic program of transcriptional repression. 

Retracted: No

PubPeer comments:
 Figure 5G. https: imgur.com 7rheLwG ,
Bladder cancer cell-derived exosomes inhibit tumor cell apoptosis and induce cell proliferation in vitro
Authors: Chun-Li Luo
Li-Xue Chen
Xiao-Hou Wu
Dan Wang
Lin Yang
Journal: Molecular Medicine Reports (2013)
Discipline: CLINICAL MEDICINE
Keywords: Exosomes; Bladder cancer; Cell viability; Apoptosis; Molecular events
Affiliations: Department of Urology, The First Affiliated Hospital of Chongqing Medical University, Yuzhong, Chongqing 400016, P.R. China.

Abstract:  Exosomes are small membrane vesicles released by a variety of mammalian cells into the extracellular space and are involved in cell‑to‑cell signaling. This study aimed to investigate the effects of bladder cancer cell‑derived exosomes on the regulation of tumor cell viability and apoptosis, as well as the underlying molecular events. Exosomes were purified from the supernatants of human bladder cancer T24 cell cultures. Transmission electron microscopy was used to confirm their morphology and western blot analyses determined the protein content of cells. Subsequently, bladder cancer cell lines were treated with different concentrations of exosomes. Tumor cell viability was shown to be reduced, as detected by the Cell Counting Kit‑8 assay. Annexin V/flow cytometric assays showed that exosomes inhibited apoptosis of bladder cancer cell lines in a dose- and time‑dependent manner. Exosomes were demonstrated to upregulate the expression of Bcl‑2 and Cyclin D1 proteins, but reduce the levels of Bax and caspase‑3 proteins in these cells. Moreover, exosomes dose‑dependently increased the expression of phosphorylated Akt and extracellular signal‑regulated protein kinase (ERK). In conclusion, this study demonstrated that bladder cancer cell‑derived exosomes inhibited tumor cell apoptosis, which was associated with the activation of Akt and ERK pathway genes, suggesting that tumor‑derived exosomes are involved in bladder cancer progression. Inhibition of exosome formation and release may therefore be a novel strategy in future treatment of bladder cancer. 

Retracted: No

PubPeer comments:
 There are many concerns about the integrity of 172 publications by this research group, including this one. Some of the concerns are published 1. Anaesthesia 2020;75:1683u201392, see Supplementary data. This paper is A144 2. Account Res 2020;28:149-61. 3. J Clin Epidemiol 2021;131:22-29. Journals and publishers were notified of these concerns in July 2019. 18 publications have an expression of concern, and 6 have been retracted. To our knowledge there has been no public response about any of the concerns. We think these publications are unreliable ,
A Fluorescent Zn(II)-Coordination Polymer: Selective Detection of Nitrofurantoin and Prevention of Peri-Implantitis after Ultrafine-Grained Titanium Implant by Reducing Inflammatory Cytokines Release
Authors: Yanxia Chi
Mingda Liu
Journal: Journal of Fluorescence (2020)
Discipline: CHEMISTRY
Keywords: Bifunctional ligand; Coordination polymer; Nitrofurantoin detection; Peri-implantitis; Zn-complex.
Affiliations: Jiamusi University, Jiamusi, Heilongjiang, China., Jiamusi University, Jiamusi, Heilongjiang, China. .

Abstract:  In the current research, a novel coordination polymer (CP) containing Zn(II) ions as nodes with the chemical formula of [Zn(IPT)2]n (1) has been produced via reaction of Zn(NO3)2·6H2O with 5-(3-(1H-imidazol-1-yl)phenyl)-1H-tetrazolate (HIPT), a heterotopic imidazole-tetrazole-bifunctional ligand. The as-prepared complex 1 has been charactered via single crystal X-ray diffraction, elemental analysis, powder X-ray diffraction (PXRD), thermogravimetric analysis (TGA) and fourier transform infrared spectroscopy (FT-IR). Because of its outstanding luminescent performances and stability, the synthesized complex 1 is a kind of excellent material of luminescent sensor of nitrofurantoin (NFT) in the water. The value of Ksv for the complex 1 to NFT is about 1.4 × 104 M-1. For the treatment of the peri-implantitis with complex 1, the ELISA test was carried out to determine the levels of the inflammatory cytokines released into the gingival crevicular fluid. The results showed that the levels of the inflammatory cytokines could be significantly reduced by complex 1 treatment. In addition to this, the real time RT-PCR was also conducted, and the data suggested the signaling pathway of TLR-4-NF-κB activation was inhibited by complex 1. 

Retracted: No

PubPeer comments:
 This SSRN preprint appears to be computer-generated with [SCIgen] . ![file] --- ![file] --- ![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). ,
A class III PDZ binding motif in the myotilin and FATZ families binds enigma family proteins: a common link for Z-disc myopathies
Authors: Anna Belgrano
Pernilla von Nandelstadh
Ivano Zara
Chiara Gardin
Mohamed Ismail
Georgine Faulkner
Giorgio Valle
Heli Suila
Olli Carpen
Journal: Molecular and Cellular Biology (2009)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Z-disc proteins; muscle disorders; myotilin; FATZ; calsarcin
Affiliations: Department of Pathology and Neuroscience Program, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland., Muscle Molecular Biology, International Centre for Genetic Engineering and Biotechnology, Padriciano 99, 34012 Trieste, Italy, Department of Biology and CRIBI Biotechnology Centre, University of Padova, Via Ugo Bassi 58b, 35131 Padua, Italy, Department of Pathology and Neuroscience Program, Biomedicum Helsinki, P.O. Box 63, Haartmninkatu 8, 00014 University of Helsinki, Helsinki, Finland, Department of Pathology, University of Turku and Turku University Central Hospital, Kiinamyllynkatu 10, 20520 Turku, Finland

Abstract:  Interactions between Z-disc proteins regulate muscle functions and disruption of these interactions results in muscle disorders. Mutations in Z-disc components myotilin, ZASP/Cypher, and FATZ-2 (calsarcin-1/myozenin-2) are associated with myopathies. We report here that the myotilin and the FATZ (calsarcin/myozenin) families share high homology at their final C-terminal five amino acids. This C-terminal E[ST][DE][DE]L motif is present almost exclusively in these families and is evolutionary conserved. We show by in vitro and in vivo studies that proteins from the myotilin and FATZ (calsarcin/myozenin) families interact via this novel type of class III PDZ binding motif with the PDZ domains of ZASP/Cypher and other Enigma family members: ALP, CLP-36, and RIL. We show that the interactions can be modulated by phosphorylation. Calmodulin-dependent kinase II phosphorylates the C terminus of FATZ-3 (calsarcin-3/myozenin-3) and myotilin, whereas PKA phosphorylates that of FATZ-1 (calsarcin-2/myozenin-1) and FATZ-2 (calsarcin-1/myozenin-1). This is the first report of a binding motif common to both the myotilin and the FATZ (calsarcin/myozenin) families that is specific for interactions with Enigma family members. 

Retracted: No

PubPeer comments:
 Figure 3C appears to have a repeated feature. *** Inverse, contrast enhanced ![file] *** Original ![file] *** Visible splice ![file] ,
Long noncoding RNA AFAP1-AS1 promotes osteosarcoma progression by regulating miR-497/IGF1R axis
Authors: Long Tan
Dan Fei
Xiaona Zhang
Yang Lu
Mingzhu Xu
Yang Zhang
Journal: American journal of translational research (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: AFAP1-AS1 miR-497; IGF1R; LncRNA; osteosarcoma.
Affiliations: Department of Ultrasonographic, The Third Hospital of Jilin University Changchun 130033, P. R. China., Department of Anesthesiology, The First Hospital of Jilin University Changchun 130021, P. R. China., Department of Nephrology, The Third Hospital of Jilin University Changchun 130033, P. R. China., Department of Neurosurgery, The First Hospital of Jilin University Changchun 130021, P. R. China.

Abstract:  Long non-coding RNA (lncRNA) actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been reported to be involved in the progression of multiple cancers. However, exact function and regulatory mechanism of AFAP1-AS1 in osteosarcoma (OS) remain largely unclear. In this study, quantitative real time polymerase chain reaction (qRT-PCR) revealed that AFAP1-AS1 was upregulated in OS tissues and cell lines. Increased AFAP1-AS1 was associated with poor prognosis. Loss-of-function experiments demonstrated that knockdown of AFAP1-AS1 inhibited the proliferation, colony formation, migration, invasion and induced cell apoptosis. Bioinformatics analysis and luciferase reporter assays confirmed that mircoRNA-497 (miR-497) was a directly target of AFAP1-AS1. Rescue experiments confirmed that miR-497 inhibition could partially reverse the inhibitory effect of AFAP1-AS1 knockdown on OS cells. Moreover, AFAP1-AS1 modulated the expression of insulin-like growth factor 1 receptor (IGF1R, a target of miR-497) indirectly. In vivo xenograft tumor assay showed that AFAP1-AS1 knockdown inhibited tumor tumorigenesis. Taken together, these findings indicate that AFAP1-AS1 promotes OS progression by regulating miR-497/IGF1R axis, providing a therapeutic target for OS. 

Retracted: No

PubPeer comments:
 Fig 7B.  Representative images of formed tumors that were subcutaneously injected with U2OS cells stable transfected with sh-AFAP1-AS1 and sh-NC plasmid. ![file] One tumor seems to have been cloned. The ruler may also be a close relative of the one seen in Fig 7B of [Zhang et al(2019)] : ![] and in Fig 6B of [Wen et al (2020)] .  Tumor images was captured at the end of the experiments . ![] , 
 *[left]* Fig 2C.  AFAP1-AS1 knockdown inhibited colony formation of U2OS cells . *[right]* Fig 2c from [Sui et al (2020)] .  Cell colony formation was determined in TPCu20101 cells transfected with shu2010NC or shu2010SNHG3 . ![file] Different experiments; one panel is shared (with a 180-deg flip). ,
Bardet–Biedl syndrome: beyond the cilium
Authors: Philip L Beales
Jonathan L Tobin
Journal: Pediatric Nephrology (2007)
Discipline: CLINICAL MEDICINE
Keywords: Bardet-Biedl syndrome; genetic cause; renal failure; children; primary cilia dysfunction
Affiliations: Molecular Medicine Unit, UCL Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.

Abstract:  The Bardet-Biedl syndrome (BBS) is a significant genetic cause of chronic and end-stage renal failure in children. Despite being a relatively rare recessive condition, BBS has come to prominence during the past few years owing to revelations of primary cilia dysfunction underlying pathogenesis. The study of this multi-system disorder, which includes obesity, cognitive impairment, genito-urinary tract malformations and limb deformities, is beginning to reveal insights into several aspects of mammalian development and organogenesis. Involvement of BBS proteins in disparate pathways such as the non-canonical Wnt and Sonic Hedgehog pathways is highlighting their interplay in disease pathogenesis. Here we review the recent developments in this emerging field, with the emphasis on the renal component of the syndrome and potential future directions. 

Retracted: No

PubPeer comments:
 I am surprised to read: ![file] To the best of my knowledge, there is only one case of patient with Bardet-Biedl syndrome associated with corpus callosum agenesis (see Karmous-Benailly et al. Am J Hum Genet 2005;76:493-504 and Keppler-Noreuil et al. BMC Medical Genet 2011;12:101). This should be corrected in the journal. ,
The DNA polymerase domain of pol(epsilon) is required for rapid, efficient, and highly accurate chromosomal DNA replication, telomere length maintenance, and normal cell senescence in Saccharomyces cerevisiae
Authors: Sakie Kanbara
Akiko Suzuki
Tomoko Ohya
Akio Sugino
Naomi Nakashima
Shin-Ichiro Hiraga
Yasuo Kawasaki
Kou Nakajo
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Saccharomyces cerevisiae; POL2; DNA polymerase epsilon; cellular functions; polymerase domain
Affiliations: Department of Biochemistry and Molecular Biology, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.

Abstract:  Saccharomyces cerevisiae POL2 encodes the catalytic subunit of DNA polymerase epsilon. This study investigates the cellular functions performed by the polymerase domain of Pol2p and its role in DNA metabolism. The pol2-16 mutation has a deletion in the catalytic domain of DNA polymerase epsilon that eliminates its polymerase and exonuclease activities. It is a viable mutant, which displays temperature sensitivity for growth and a defect in elongation step of chromosomal DNA replication even at permissive temperatures. This mutation is synthetic lethal in combination with temperature-sensitive mutants or the 3'- to 5'-exonuclease-deficient mutant of DNA polymerase delta in a haploid cell. These results suggest that the catalytic activity of DNA polymerase epsilon participates in the same pathway as DNA polymerase delta, and this is consistent with the observation that DNA polymerases delta and epsilon colocalize in some punctate foci on yeast chromatids during S phase. The pol2-16 mutant senesces more rapidly than wild type strain and also has shorter telomeres. These results indicate that the DNA polymerase domain of Pol2p is required for rapid, efficient, and highly accurate chromosomal DNA replication in yeast. 

Retracted: No

PubPeer comments:
 1.The ARS1 bands in Figure 2A and Figure 2B (Red boxes) were similar, only with different exposure time. 2.The backgrounds of ARS501 in Figure 2A and Figure 2B (Blue boxes) were similar, with different exposure time. ![file] ,
miR-363 inhibits the growth, migration and invasion of hepatocellular carcinoma cells by regulating E2F3
Authors: Kai Liu
Junfeng Ye
Songyang Liu
Wei Zhang
Yahui Liu
Journal: Oncology Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: microRNA-363; tumor progression; hepatocellular carcinoma; chemotherapeutic drugs; biological function
Affiliations: Department of Hepatopancreatobiliary Surgery, The First Hospital of Jilin University, Changchun, Jilinï¿½130021, P.R.ï¿½China

Abstract:  A growing body of evidence suggests that microRNA-363 (miR-363) plays crucial roles in tumor progression, development and metastasis, and confer resistance to chemotherapeutic drugs in several types of cancers. However, the biological function and underlying molecular mechanism of miR-363 in hepatocellular carcinoma (HCC) have not been fully elucidated. In the present study, we investigated the biological function and mechanism of miR-363 in the regulation of HCC progression. We found that miR-363 was downregulated in HCC cell lines and tissues, and a low expression level of miR-363 was associated with tumor differentiation, TNM stage and lymph node metastasis. Forced overexpression of miR-363 significantly suppressed HCC cell proliferation, migration, invasion and decreased epithelial‑mesenchymal transition (EMT) in vitro, as well as inhibited tumor growth in vivo. Analysis of the underlying mechanisms revealed that miR-363 regulated E2F transcription factor 3 (E2F3) expression by directly targeting its 3' untranslated region. E2F3 overexpression partially attenuated the tumor-suppressive effects of miR-363 in HCC cells. In addition, E2F3 expression was upregulated in the HCC tissues, and was negatively correlated with the level of miR-363 in human HCC tissues. Taken together, these results revealed that miR-363 is involved in HCC growth and invasion and functions as a tumor suppressor by negatively regulating E2F3. 

Retracted: Yes

PubPeer comments:
 *[left]* Fig 2E.  Image of tumor tissues of each group . *[right]* Fig 3C from [Qiu et al (2016)] .  Representative photograph of xenograft tumors . ![file] Could the authors of either paper comment on the number of tumors appearing in both? UPDATE: Fig 6B from [Jing et al (2019)] .  The tumor image . ![file] , 
 Retracted [6 September 2021] . ------------------------------ Following the publication of this paper, it was drawn to the Editorsu2019 attention by a concerned reader that tumour images featured in Fig. 2E were strikingly similar to those that had already appeared in different form in another article by different authors at different research institutes. Owing to the fact that the contentious data in the above article had already been published elsewhere prior to its submission to *Oncology Reports*, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. ,
Neuroprotective efficacy of hesperetin against cadmium induced oxidative stress in the brain of rats
Authors: Kalist Shagirtha
Selvaraj MiltonPrabu
Nazima Bashir
Journal: Toxicology and industrial health (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: ATPases; Hesperetin; antioxidants; brain; cadmium
Affiliations: Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamilnadu, India, Department of Zoology, Faculty of Science, Annamalai University, Annamalainagar, Tamilnadu, India

Abstract:  The present study was designed to investigate the neuroprotective effect of hesperetin (Hp) against cadmium (Cd)-induced neurotoxicity in rats. Cadmium (3 mg/kg body weight (b.w.), subcutaneous) administration for 3 weeks demonstrated neurotoxicity in rats by the decreased activity of acetylcholinesterase in the brain. The oxidative stress markers (thiobarbituric acid reactive substances and protein carbonyls) were significantly increased with decreased enzymatic (superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase) and non-enzymatic antioxidants (reduced glutathione, total sulphydryl groups and vitamin C). The proteolytic and membrane-bound enzymes (Na+ K+-ATPase, Mg2+-ATPase and Ca2+-ATPase) were also decreased with increased apoptotic markers (Bcl2 Associated X Protein (Bax), cytochrome C, caspase 3 and 9) and decreased anti-apoptotic marker (B-cell lymphoma 2 (Bcl2)) in the brain of Cd-treated rats. Moreover, Cd administration significantly decreased the mitochondrial electron transport chain complexes (I, II, III and IV) in the brain of rats. Preadministration of Hp (40 mg/kg b.w., oral) significantly attenuated the Cd-induced oxidative stress and mitochondrial dysfunction, restored the antioxidant and membrane-bound enzyme activities and decreased apoptosis in the brain of rats. 

Retracted: No

PubPeer comments:
 Concern about Figure 6. Panel C appears to have an unexpected small repeat. Highlighted with green boxes. Could the authors explain what happened here, please? ![file] ,
MicroRNAs-491-5p suppresses cell proliferation and invasion by inhibiting IGF2BP1 in non-small cell lung cancer
Authors: Ping Ren
Fangchao Gong
Hong Zhang
Yan Zhang
Jindong Jiang
Journal: American journal of translational research (2016)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: IGF2BP1; Non-small lung cancer; invasion; miR-491-5p; proliferation.
Affiliations: Department of Thoracic Surgery, The First Hospital, Jilin University 71 Xinming Street, Chaoyang District, Changchun 130021, China.

Abstract:  MicroRNAs-491-5p (miR-491-5p) has been found to involve in tumor initiation and development in several tumors. However, the biological function and underlying molecular mechanism of miR-491-5p in non-small lung cancer (NSCLC) remain unclear. This study was therefore to investigate biological role of and underlying molecular mechanisms of in NSCLC. It was found that miR-491-5p expression was significantly downregulated in NSCLC tissues when compared with corresponding adjacent normal tissues (P&lt;0.01), and the value was negatively related to advanced and tumor-node-metastasis (TNM) stage and lymph node metastasis (both P&lt;0.01). We also demonstrate that restoration of miR-491-5p suppressed NSCLC cell proliferation by arresting NSCLC cells in the G1/G0 phase and accelerating apoptosis. miR-491-5p also inhibited cell migration and invasion in NSCLC cells. Mechanically, IGF2BP1 was identified as direct targets of miR-491-5p. And IGF2BP1 expression was significantly upregulated, and correlated negative with miR-491-5p expression in NSCLC tissues. In vivo assay showed thatmiR-491-5p suppressed tumor growth in nude model by repressing IGF2BP1 expression. Collectively, miR-491-5p functioned as a tumor suppressor in NSCLC by targeting IGF2BP1. Restoration of miR-491-5p expression may represent a promising therapeutic approach for targeting malignant NSCLC. 

Retracted: No

PubPeer comments:
 *[left]* Fig 5B.  IGF2BP1 ... protein expression in human NSCLC tissues and their corresponding normal tissues were determined by ... western blot . *[right]* Fig 6D.  Detection of IGF2BP1 protein expression in tumor tissues by Western blot , with one band flipped. ![file] Figure 6 from [Wu et al (2015)] .  miR-128 regulates AKT signaling pathway and its downstream gene. Western blotting determined AKT, p-AKT, cyclin D1, Bcl-2 and MMP-2 protein expression in SW480 cells transfected with miR-128 mimic or miR-NC. u03b2-actin was used as an internal control , with two bands flipped or rotated. ![file] Some remarkable similarities. , 
 Now with different colors! Fig 5B at left; Figure 6 from Wu et al (2015) at right; in the middle, Figs 4C, 5D from [Zhou et al (2016)] .  hTERT protein expression in HeLa cells transfected with miR-138 mimic were detected by western blot analysis ;  hTERT was determined by western blot analysis. ![file] How does this happen? ,
Antitumor Molecular Mechanism of Chlorogenic Acid on Inducting Genes GSK-3 β and APC and Inhibiting Gene β -Catenin
Authors: Xiaoping Xu
Jie Ren
Ruoshi Xu
Qiumei Kang
Zukun Li
Journal: Journal of Analytical Methods in Chemistry (2013)
Discipline: CHEMISTRY
Keywords: gene inhibition; Wnt pathway; chlorogenic acid; apoptosis; GSK-3 β
Affiliations: West China School of Stomatology, Sichuan University, Chengdu, Sichuan 610041, China., West China School of Pharmacy, Sichuan University, Chengdu, Sichuan 610041, China

Abstract:  Objective. Inhibiting gene β -catenin and inducting genes GSK-3 β and APC, promoting the tumor cell apoptosis in Wnt pathway, by chlorogenic acid were discussed (CGA). Method. The different genes were scanned by the 4∗44K mouse microarray chips. The effect of the three genes was confirmed by RT-PCR technique with CGA dosage of 5, 10, and 20 mg/kg. Result. The expression of GSK-3 β and APC was upregulated in group of 20 mg/kg dosage (P &lt; 0.05) and the expression of β -catenin was downregulated in the same dosage (P &lt; 0.05). Conclusion. The results infer that the multimeric protein complex of β -catenin could be increased by CGA upregulated genes GSK-3 β and APC, which could inhibit the free β -catenin into the nucleus to connect with TCF. So the transcriptional expression of the target genes will be cut to abnormal cell proliferation. It is probably one of the ways that can stop the tumor increase by CGA. 

Retracted: No

PubPeer comments:
 2021 retraction. https: www.hindawi.com journals jamc 2021 5414158 Journal of Analytical Methods in Chemistry has retracted the article titled u201cAntitumor Molecular Mechanism of Chlorogenic Acid on Inducting Genes GSK-3u03b2 and APC and Inhibiting Gene u03b2-Cateninu201d [1]. Confidential information from Sichuan Jiuzhang Biological Science and Technology Co., Ltd. (previously known as Sichuan Jiuzhang Biochemical Engineering Science and Technology Development Co., Ltd.) was published without permission, as confirmed by a court judgment. A previous corrigendum that acknowledged the involvement of the company was not sufficient [2]. References R. Xu, Q. Kang, J. Ren, Z. Li, and X. Xu, u201cAntitumor Molecular Mechanism of Chlorogenic Acid on Inducting Genes GSK-3u03b2 and APC and Inhibiting Gene u03b2-Catenin,u201d Journal of Analytical Methods in Chemistry, vol. 2013, Article ID 951319, 7 pages, 2013. R. Xu, Q. Kang, J. Ren, Z. Li, and X. Xu, u201cCorrigendum to u201cantitumor molecular mechanism of chlorogenic acid on inducting genes GSK- 3 and APC and inhibiting gene u03b2-catenin,u201d Journal of Analytical Methods in Chemistry, vol. 2015, Article ID 189328, p. 1, 2015. ,
MicroRNA-378 promotes the malignant progression of oral squamous cell carcinoma by mediating FOXN3
Authors: M Luo
N Ding
X-L Liao
Q-Y Bao
B Wu
R-Y Li
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: microRNA-378; OSCC; clinicopathology; prognosis; RT-qPCR
Affiliations: Department of Stomatology, Beijing LuHe Hospital Capital Medical University, Beijing, China. .

Abstract:  Objective: This study aimed to detect the expression of microRNA-378 in OSCC, and further studies its effects on clinicopathology and prognosis of OSCC patients. Patients and methods: Real-Time quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect the expression levels of microRNA-378 in 96 pairs of OSCC tissues and paracancerous tissues. The relationship between microRNA-378 expression and pathological parameters and prognosis of OSCC patients was analyzed. The expression level of microRNA-378 in OSCC cells was detected by RT-qPCR as well. Also, microRNA-378 knockdown expression model was constructed using small interfering RNA in OSCC cell lines CAL-27 and Tca8113. Biological functions of OSCC cells were determined using cell counting kit-8 (CCK-8), colony formation, and transwell assay. Western blot was conducted to detect the protein expression of FOXN3 in OSCC cells. Results: RT-qPCR results showed that the expression level of microRNA-378 in OSCC tissues is remarkably higher than that in paracancerous tissues. Compared with OSCC patients with lower expression of microRNA-378, patients with higher expression of microRNA-378 had higher incidences of lymph node metastasis and distant metastasis, as well as shorter overall survival. MicroRNA-378 knockdown significantly decreased proliferative, invasive, and metastatic abilities of OSCC cells. Western blot results showed that microRNA-378 downregulates FOXN3 expression in OSCC cells. Rescue experiments found that microRNA-378 could regulate FOXN3, thus promoting the malignant progression of OSCC. Conclusions: MicroRNA-378 is highly expressed in OSCC, which is significantly associated with tumor staging, distant metastasis, and poor prognosis of OSCC. It is shown that microRNA-378 may promote malignant progression of OSCC by regulating FOXN3. 

Retracted: No

PubPeer comments:
 Fig 1D.  Kaplan-Meier survival curves of OSCC patients based on their microRNA-378 expressions. Patients in the high expression group had an unfavorable prognosis than those in the low expression group . ![file] Another manifestation of Hoya s Law for J.BUOn and ERMPS...  When 40 or 50 cases of any given cancer are dichotomised into half-groups of high- or low-expression of any given nc-RNA, survival rate for one half-group or both will drop to 0% at 75 months. Other examples, from left to right: - Fig 1 from [Zang et al (2020)] - Fig 1 from [Li et al (2020)] - Fig 1, and Fig 4D, from [Cui et al (2019)] - Fig 1D from [Gao et al (2019)] . ![file] *[left]* Figure 1C from [Wu et al (2020)] . *[right]* Figs 1D, 3E from [Wu et al (2019)] . ![file] ,
Antitumor activity of di-n-butyl-(2,6-difluorobenzohydroxamato)tin(IV) against human gastric carcinoma SGC-7901 cells via G2/M cell cycle arrest and cell apoptosis
Authors: Li Qingshan
Li Yunlan
Zheng Juan
Journal: PLoS ONE (2014)
Discipline: Multidisciplinary
Keywords: DBDFT; antitumor agent; G2/M phase; cell cycle; apoptosis
Affiliations: School of Pharmaceutical Science, Shanxi Medical University, Taiyuan, People's Republic of China.

Abstract:  Di-n-butyl-(2,6-difluorobenzohydroxamato)Tin(IV) (DBDFT), a potential antitumor agent against malignancies, exhibited high activities both in vitro and in vivo. Flow cytometric analysis showed that treatment with DBDFT against Human Gastric Carcinoma (SGC-7901) cells induced a concentration and time-dependent cell accumulation in the G2/M phase of the cell cycle with a parallel depletion of the percentage of cells in G0/G1, the cell apoptosis was observed by characteristic morphological changes and AnnexinV/PI dual-immunofluorescence staining. Fluorescence quantitative FQ- PCR and western blot results showed that G2/M-phase arrest was correlated with up-regulation of cyclin dependent kinase inhibitor p21, Chk2 and CyclinB1, whereas the expressions of other G2/M regulatory check-point protein, Cdc2, and feedback loop protein Cdc25C were obviously down-regulated in a p53-independent manner after the SGC-7901 cells were treated with DBDFT (2.5, 5.0, 7.5 µmol·L(-1)) compared with the control. Furthermore, the up-regulation of Bax and down-regulation of Bcl-2 as well as the activation of caspase-3 were observed, which indicated that DBDFT treatment triggered the mitochondrial apoptotic pathway with an increase of Bax/Bcl-2 ratios, resulting in mitochondrial membrane potential loss and caspase-9 activation in DBDFT treated SGC-7901 cells. In summary, the results illustrated the involvement of multiple signaling pathways targeted by DBDFT in mediating G2/M cell cycle arrest and apoptosis in SGC-7901 cells, which suggested that DBDFT might have therapeutic potential against gastric carcinoma as an effective compound. 

Retracted: No

PubPeer comments:
 Figure 6C and Figure 8B * In both figures and in most panels, lanes 0 and 2.5 umol l for 24 h look similar to 0h and 24h, which are not quite the same experiments. Lanes are represented as having run on the same blot, but appear to be rearranged. Boxes of the same color show lanes that look similar. Reported to the journal in October 2015, but no action taken as of today. ![file] ,
SOX15 regulates proliferation and migration of endometrial cancer cells
Authors: Xiping Jiang
Jingting Jiang
Yun Xu
Xiaohui Rui
Caixia Guo
Journal: Bioscience Reports (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SOX15; endometrial cancer; migration; proliferation.
Affiliations: Department of Gynecology, Changzhou First People's Hospital, Changzhou, Jiangsu 213003, China., Tumor Biological Treatment Center of Changzhou First People's Hospital, Changzhou, Jiangsu 213003, China .

Abstract:  The study aimed to investigate the effects of Sry-like high mobility group box 15 (SOX15) on proliferation and migration of endometrial cancer (EC) cells. Immunohistochemistry (IHC) was applied to determine the expression of SOX15 in EC tissues and adjacent tissues. We used cell transfection method to construct the HEC-1-A and Ishikawa cell lines with stable overexpression and low expression SOX15 Reverse-transcription quantitative real-time PCR (RT-qPCR) and Western blot were performed to examine expression of SOX15 mRNA and SOX15 protein, respectively. By conducting a series of cell proliferation assay and migration assay, we analyzed the influence of SOX15 overexpression or low expression on EC cell proliferation and migration. The expression of SOX15 mRNA and protein in EC tissues was significantly lower than that in adjacent tissues. After lentivirus-transfecting SOX15, the expression level of SOX15 mRNA and protein was significantly increased in cells of SOX15 group, and decreased in sh-SOX15 group. Overexpression of SOX15 could suppress cell proliferation, while down-regulation of SOX15 increased cell proliferation. Flow cytometry results indicated that overexpression of SOX15 induced the ratio of cell-cycle arrest in G1 stage. In addition, Transwell migration assay results showed that SOX15 overexpression significantly inhibited cell migration, and also down-regulation of SOX15 promoted the migration. As a whole, SOX15 could regulate the proliferation and migration of EC cells and up- regulation of SOX15 could be valuable for EC treatment. 

Retracted: Yes

PubPeer comments:
 figure 3a ![file] , 
 Retracted [16 April 2021](10.1042 BSR-20171045_RET). ---------------------------------------------- This article is being retracted from Bioscience Reports at the request of the Editor-in-Chief and the Editorial Board following receipt of a notification from a reader, alerting the Editorial Board to three pairs of duplicated images in Figure 3A. The authors were contacted regarding the concerns raised and provided a replacement Figure 3A, however given the number of duplicated images and the resizing of the images, the Editorial Board stands by the decision to retract. The authors agree to the retraction. ,
Long non-coding RNA CRNDE sponges miR-384 to promote proliferation and metastasis of pancreatic cancer cells through upregulating IRS1
Authors: Yajun Wei
Gang Wang
Lu Zhang
Jingen Pan
Cheng Wang
Journal: Cell Proliferation (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Colorectal neoplasia differentially expressed (CRNDE); long non-coding RNA (lncRNA); pancreatic cancer; expression levels; clinicopathologic characteristics
Affiliations: Department of Biliary and Pancreatic Surgery; Anhui Provincial Hospital Affiliated with Anhui Medical University; Hefei Anhui China

Abstract:  Objective: Colorectal neoplasia differentially expressed (CRNDE), a vital cancer-related long non-coding RNA (lncRNA), has been brought to reports for playing quintessential functions in the growth and progression of several human malignancies. Nevertheless, the expression as well as the functional mechanisms of CRNDE in pancreatic cancer is not known so for. This study aimed at investigating the biological and clinical importance of CRNDE in human pancreatic cancer. Materials and methods: The expression levels of CRNDE in pancreatic cancer tissues as well as cell lines were identified with the help of quantitative real-time PCR (qRT-PCR). Furthermore, the analysis of the relationship between CRNDE expression and clinicopathologic characteristics of patients with pancreatic cancer was also performed. Novel target of CRNDE was identified with the use of bioinformatics analysis and confirmed by a dual-luciferase reporter assay. Colorectal neoplasia differentially expressed was knocked down using siRNA in pancreatic cancer cells. Thereafter, cell proliferation, migration and invasion were examined. Tumour xenograft was created to explore the function of CRNDE in tumorigenesis in vivo. Results: Upregulation of the expression of CRNDE was found in pancreatic cancer tissues as well as cell lines, in comparison with the adjacent non-tumour tissues and human pancreatic duct epithelial cells. High expression of CRNDE was correlated with poor clinicpathological characteristics and shorter overall survival. We identified miR-384 as a direct target for CRNDE. Moreover, the CRNDE knockdown considerably inhibited pancreatic cancer cell proliferation, migration and invasion not only in vitro but also in vivo. In addition, CRNDE positively regulated IRS1 expression through sponging miR-384. Conclusions: Colorectal neoplasia differentially expressed performed an oncogenic function in cell proliferation as well as metastasis of pancreatic cancer. Our results suggest that CRNDE is likely to serve as an efficient therapeutic approach in respect of pancreatic cancer treatment. 

Retracted: No

PubPeer comments:
 The micrographs in Figure 2 and 4 appear to have been put together in a randomly fashion, and the science totally forgotten. I detected four cases of data duplication manipulation after a quick check. ![file] ,