PReD-Bench/PRed-Bench huggingface dataset:
MiR-374b targets GATA3 to promote progression and development of glioblastoma via regulating SEMA3B
Authors: S Bai
Y Wang
S Zhao
R Wang
Z He
J Gao
Journal: Neoplasma (2019)
Discipline: CLINICAL MEDICINE
Keywords: miR-374b; GATA3; SEMA3B; glioma; cell viability
Affiliations: Department of Image Diagnostics, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China., Department of Dermatology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China., Department of Clinical Laboratory, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China., Department of Neurosurgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.

Abstract:  In the present study, a series of studies were conducted to explore the function of miR-374b in glioma and the regulatory relationship among miR-374b, GATA3 and SEMA3B. In the present study, miR-374b mimics and inhibitors were employed to regulate miR-374b expression. Besides, qRT-PCR assay was used for detecting the expression level of miR-374b, GATA3 and SEMAB mRNAs. To verify the targeting relationship between miR-374b and GATA3, dual luciferase analysis was utilized. Moreover, chromatin immunoprecipitationn (ChIP) assay was performed for identify the correlation of GATA3 with SEMA3B. Furthermore, si1-GATA3, si2-GATA3 and pc-GATA3 were used to regulate GATA3 expression, and pc-SEMA3B was taken advantage for dysregulating SEMA3B. For assessing the significance of miR374b alone or co-operated with GATA3 or SEMA3B in cell viability, migration and apoptosis, CCK-8, transwell and FCM assay were performed, respectively. We found that overexpression of miR-374b, which was identified in glioma tissues and cell lines, U251, LN-299 and GOS-3, promoting cell migration and enhancing cell viability but inhibiting cell apoptosis were suggested in this research. Besides, GATA3 contributed to increase in cell viability and migration and decrease in cell apoptosis targeted by miR-374b as evidenced by dual luciferase assay. Moreover, GATA3 binding to the promoter of SEMA3B involved in regulating SEMA3B was revealed. Further, a series of studies demonstrated that miR-374b targeting GATA3 regulating SMEA3B resulted in elevation in cell viability and migration but suppression in cell apoptosis. But the promotion effects of miR-374 in glioma process were reversed by co-transfecting pc-GATA3 or pc-SEMA3B. In conclusion, miR-374b promotes glioma process in vitro through suppressing SEMA3B via targeting GATA3. The result of this study provides an important clue to the optimal treatment schedule for glioblastoma. 

Retracted: No

PubPeer comments:
 In Figure 2E, a micrograph has been duplicated and presented as something else (Blank vs NC). ![file] ,
MicroRNA-21 modulates the levels of reactive oxygen species by targeting SOD3 and TNFα
Authors: Linlin Tian
Wooi-Loon Ng
Ping Wang
Ya Wang
Huichen Wang
Paul Doetsch
Xiangming Zhang
Erica Werner
Journal: Cancer Research (2012)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNA-21; oncomir; human tumors; malignant growth; progression
Affiliations: Department of Radiation Oncology, Winship Cancer Institute, Emory University School of Medicine, Emory University, Atlanta, Georgia 30322, USA.

Abstract:  MicroRNA-21 (miR-21) is an oncomir overexpressed in most human tumors in that it promotes malignant growth and progression by acting on multiple targets. Here, we broaden the impact of miR-21 in cancer by showing that it regulates the formation of reactive oxygen species (ROS) that promote tumorigenesis. Key targets of miR-21 in mediating this function were SOD3 and TNFα. We found that miR-21 inhibited the metabolism of superoxide to hydrogen peroxide, produced either by endogenous basal activities or exposure to ionizing radiation (IR), by directing attenuating SOD3 or by an indirect mechanism that limited TNFa production, thereby reducing SOD2 levels. Importantly, both effects contributed to an elevation of IR-induced cell transformation. Our findings, therefore, establish that miR-21 promotes tumorigenesis to a large extent through its regulation of cellular ROS levels. 

Retracted: No

PubPeer comments:
 Figure 3A. Much more similar than you would expect. https: imgur.com rwIz8px , 
 https: retractionwatch.com 2021 09 16 former-emory-division-director-committed-misconduct-says-federal-watchdog ,
Tendon is covered by a basement membrane epithelium that is required for cell retention and the prevention of adhesion formation
Authors: Susan H Taylor
Yinhui Lu
Karl E Kadler
Sarah Al-Youha
Jason Wong
Duncan A McGrouther
Tom Van Agtmael
Journal: PLoS ONE (2011)
Discipline: Multidisciplinary
Keywords: tendons; fibrous adhesions; cell migration; trypsin; basement membrane
Affiliations: Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom.

Abstract:  The ability of tendons to glide smoothly during muscle contraction is impaired after injury by fibrous adhesions that form between the damaged tendon surface and surrounding tissues. To understand how adhesions form we incubated excised tendons in fibrin gels (to mimic the homeostatic environment at the injury site) and assessed cell migration. We noticed cells exiting the tendon from only the cut ends. Furthermore, treatment of the tendon with trypsin resulted in cell extravagation from the shaft of the tendons. Electron microscopy and immunolocalisation studies showed that the tendons are covered by a novel cell layer in which a collagen type IV/laminin basement membrane (BM) overlies a keratinised epithelium. PCR and western blot analyses confirmed the expression of laminin β1 in surface cells, only. To evaluate the cell retentive properties of the BM in vivo we examined the tendons of the Col4a1(+/Svc) mouse that is heterozygous for a G-to-A transition in the Col4a1 gene that produces a G1064D substitution in the α1(IV) chain of collagen IV. The flexor tendons had a discontinuous BM, developed fibrous adhesions with overlying tissues, and were acellular at sites of adhesion formation. In further experiments, tenotomy of wild-type mice resulted in expression of laminin throughout the adhesion. In conclusion, we show the existence of a novel tendon BM-epithelium that is required to prevent adhesion formation. The Col4a1(+/Svc) mouse is an effective animal model for studying adhesion formation because of the presence of a structurally-defective collagen type IV-containing BM. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
null, 
null, 
 Agreed with comments from # 1, 3 and 5, the authors should be able to provide higher quality images to answer. In addition to Figure 3D, I also see some cut in 2B... ![file] , 
 Response from the author M. Peter: As pointed out above. This kind of splicing was allowed and very common back then. Not done these days anymore. Most journals adopted new image manipulation rules about ten years ago. Some of the splicing is very obvious. It was not done to hide but to look even so not to distract from the data. ,
MicroRNA-18b inhibits the growth of malignant melanoma via inhibition of HIF-1α-mediated glycolysis
Authors: Yao Chen
Jianda Zhou
Ziqing Zhang
Chengqun Luo
Zizi Chen
Journal: Oncology Reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: MicroRNAs; miR-18b; malignant melanoma; downregulated; tumor thickness
Affiliations: Department of Plastic and Cosmetic Surgery, Longgang Orthopetics Hospital of Shenzhen, Shenzhen, Guangdong 518000. P.R. China., Department of Plastic Surgery, the Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China.

Abstract:  MicroRNAs (miRs) have been demonstrated to play critical roles in the development and progression of malignant melanoma (MM). However, the exact role and underlying mechanism of miR-18b in MM growth remains unclear. In the present study, real-time PCR data indicated that miR-18b was significantly downregulated in MM tissues compared to their matched adjacent non-tumor tissues. Low miR-18b expression was significantly associated with the tumor thickness and stage, although no significant association was observed between the miR-18b expression and the age, gender, or lymph node metastasis. Besides, miR-18b was also significantly downregulated in MM B16 and A375 cells compared to normal skin HACAT cells. Ectopic expression of miR-18b decreased the proliferation of A375 and B16 cells, while induced a remarkable cell cycle arrest at G1 stage. Besides, miR-18b overexpression also inhibited the glycolysis in A375 and B16 cells. HIF-1α, a key regulator in glycolysis, was then identified as a target gene of miR-18b, and its expression was negatively mediated by miR-18b in A375 and B16 cells. Overexpression of HIF-1α rescued the suppressive effect of miR-18b on MM cell proliferation and glycolysis. In vivo study further showed that overexpression of miR-18b inhibited the MM growth as well as the tumor-related death, accompanied with HIF-1α downregulation. Taken together, the present study suggests that miR-18b inhibits the growth of MM cells in vitro and in vivo through directly targeting HIF-1α. 

Retracted: Yes

PubPeer comments:
 The authors in Definition 6 introduced a notion called u201cN-soft setu201d. In Example 10, the authors provided a concrete example of the N-soft set, which is illustrated in Table 1 and Table 2. However, according to Table 2, **such an N-soft set is nothing but a matrix form using Likert 5-point scale.** Such an organization of data is a usual manner in decision making. **Calling such a matrix form an N-soft set introduces nothing new.** Can the authors kindly address the u201c**novelty**u201d associated with N-soft sets in this particular context of multi-attribute group decision making? ![file] ![file] ![file] ![file] ,
Phosphorylation of Slx4 by Mec1 and Tel1 regulates the single-strand annealing mode of DNA repair in budding yeast
Authors: Rachel Toth
Neal Sugawara
Sonja Flott
David G Campbell
Constance Alabert
John Rouse
Geraldine W Toh
Philippe Pasero
James E Haber
Journal: Molecular and Cellular Biology (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Budding yeast; Slx4; Sgs1 helicase; DNA damage; DNA synthesis
Affiliations: MRC Protein Phosphorylation Unit, James Black Centre, University of Dundee, Dundee DD1 5EH, United Kingdom., Institute of Human Genetics, CNRS UPR 1142, 141 Rue de la Cardonille, 34396 Montpellier, France, MRC Protein Phosphorylation Unit, James Black Centre, University of Dundee, Dundee DD1 5EH, United Kingdom, Rosenstiel Basic Medical Sciences Research Centre, Waltham, Massachusetts

Abstract:  Budding yeast (Saccharomyces cerevisiae) Slx4 is essential for cell viability in the absence of the Sgs1 helicase and for recovery from DNA damage. Here we report that cells lacking Slx4 have difficulties in completing DNA synthesis during recovery from replisome stalling induced by the DNA alkylating agent methyl methanesulfonate (MMS). Although DNA synthesis restarts during recovery, cells are left with unreplicated gaps in the genome despite an increase in translesion synthesis. In this light, epistasis experiments show that SLX4 interacts with genes involved in error-free bypass of DNA lesions. Slx4 associates physically, in a mutually exclusive manner, with two structure-specific endonucleases, Rad1 and Slx1, but neither of these enzymes is required for Slx4 to promote resistance to MMS. However, Rad1-dependent DNA repair by single-strand annealing (SSA) requires Slx4. Strikingly, phosphorylation of Slx4 by the Mec1 and Tel1 kinases appears to be essential for SSA but not for cell viability in the absence of Sgs1 or for cellular resistance to MMS. These results indicate that Slx4 has multiple functions in responding to DNA damage and that a subset of these are regulated by Mec1/Tel1-dependent phosphorylation. 

Retracted: No

PubPeer comments:
 2020 retraction. https: lipidworld.biomedcentral.com articles 10.1186 s12944-020-01281-z The Editor-in-Chief has retracted this article [1] because it significantly overlaps with a previously published article by Zheng and Mao [2]. The authors have not addressed this, despite several attempts from the Publisher. References 1. Zhou K, Cen J. The fatty liver index (FLI) and incident hypertension: a longitudinal study among Chinese population. Lipids Health Dis. 2018;17:214. https: doi.org 10.1186 s12944-018-0858-6. ,
MYC abrogates p53-mediated cell cycle arrest in N-(phosphonacetyl)-L-aspartate-treated cells, permitting CAD gene amplification
Authors: M V Chernov
O B Chernova
G R Stark
M L Agarwal
Y Ishizaka
Journal: Molecular and cellular biology (1998)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Genomic instability; gene amplification; neoplastic cells; N-(phosphonacetyl)-L-aspartate (PALA); pyrimidine nucleotides
Affiliations: Department of Molecular Biology, Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195,
1
 and, Department of Hematology, Research Institute, International Medical Center of Japan, Shinjuku-ku, Tokyo 162, Japan2

Abstract:  Genomic instability, including the ability to undergo gene amplification, is a hallmark of neoplastic cells. Similar to normal cells, "nonpermissive" REF52 cells do not develop resistance to N-(phosphonacetyl)-L-aspartate (PALA), an inhibitor of the synthesis of pyrimidine nucleotides, through amplification of cad, the target gene, but instead undergo protective, long-term, p53-dependent cell cycle arrest. Expression of exogenous MYC prevents this arrest and allows REF52 cells to proceed to mitosis when pyrimidine nucleotides are limiting. This results in DNA breaks, leading to cell death and, rarely, to cad gene amplification and PALA resistance. Pretreatment of REF52 cells with a low concentration of PALA, which slows DNA replication but does not trigger cell cycle arrest, followed by exposure to a high, selective concentration of PALA, promotes the formation of PALA-resistant cells in which the physically linked cad and endogenous N-myc genes are coamplified. The activated expression of endogenous N-myc in these pretreated PALA-resistant cells allows them to bypass the p53-mediated arrest that is characteristic of untreated REF52 cells. Our data demonstrate that two distinct events are required to form PALA-resistant REF52 cells: amplification of cad, whose product overcomes the action of the drug, and increased expression of N-myc, whose product overcomes the PALA-induced cell cycle block. These paired events occur at a detectable frequency only when the genes are physically linked, as cad and N-myc are. In untreated REF52 cells overexpressing N-MYC, the level of p53 is significantly elevated but there is no induction of p21waf1 expression or growth arrest. However, after DNA is damaged, the activated p53 executes rapid apoptosis in these REF52/N-myc cells instead of the long-term protective arrest seen in REF52 cells. The predominantly cytoplasmic localization of stabilized p53 in REF52/N-myc cells suggests that cytoplasmic retention may help to inactivate the growth-suppressing function of p53. 

Retracted: No

PubPeer comments:
 Figure 4. Much more similar than you would expect. https: imgur.com J3qOSMN , 
 Figure 7A. Much more similar than you would expect. https: imgur.com bq8Mio6 ,
MNK1-induced eIF-4E phosphorylation in myeloma cells: a pathway mediating IL-6-induced expansion and expression of genes involved in metabolic and proteotoxic responses
Authors: Carolyne Bardeleben
Bao Hoang
Patrick Frost
Alan Lichtenstein
Joseph Gera
Yijiang Shi
Yonghui Yang
Journal: PloS one (2014)
Discipline: Multidisciplinary
Keywords: Multiple myeloma; Endoplasmic reticulum stress; MAPK-interacting kinases; MNKs; Protein translation
Affiliations: Department of Medicine, Hematology-Oncology, Greater Los Angeles VA Healthcare Center, Los Angeles, California, United States of America; Department of Medicine, UCLA School of Medicine, Los Angeles, California, United States of America; Jonsson Comprehensive Cancer Center, Los Angeles, California, United States of America.

Abstract:  Because multiple myeloma (MM) cells are at risk for endoplasmic reticulum (ER) stress, they require a carefully regulated mechanism to promote protein translation of selected transcripts when proliferation is stimulated. MAPK-interacting kinases (MNKs) may provide this mechanism by enhancing cap-dependent translation of a small number of critical transcripts. We, thus, tested whether MNKs played a role in MM responses to the myeloma growth factor interleukin-6 (IL-6). IL-6 activated MNK1 phosphorylation and induced phosphorylation of its substrate, eIF-4E, in MM lines and primary specimens. MNK paralysis, achieved pharmacologically or by shRNA, prevented MM expansion stimulated by IL-6. A phosphodefective eIF-4E mutant also prevented the IL-6 response, supporting the notion that MNK's role was via phosphorylation of eIF-4E. Both pharmacological MNK inhibition and expression of the phosphodefective eIF-4E mutant inhibited MM growth in mice. Although critical for IL-6-induced expansion, eIF-4E phosphorylation had no significant effect on global translation or Ig expression. Deep sequencing of ribosome-protected mRNAs revealed a repertoire of genes involved in metabolic processes and ER stress modulation whose translation was regulated by eIF-4E phosphorylation. These data indicate MM cells exploit the MNK/eIF-4E pathway for selective mRNA translation without enhancing global translation and risking ER stress. 

Retracted: No

PubPeer comments:
 Figure 1. Much more smilar than you would expect. https: imgur.com 9zw3pzZ ,
LATS2 suppresses oncogenic Wnt signaling by disrupting β-catenin/BCL9 interaction
Authors: Razqallah Hakem
Khalid Al Hezaimi
Zhi-Chun Lai
Jiong Li
Yingduan Cheng
Bin Zhao
Kun-Liang Guan
Xiangming Ding
Cun-Yu Wang
Xiaohong Chen
Journal: Cell reports (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Wnt/β-catenin; LATS2; BCL9; transcription; colorectal cancers
Affiliations: Laboratory of Molecular Signaling, Division of Oral Biology and Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA., Department of Otolaryngology and Head and Neck Surgery, Affiliated Beijing Tongren Hospital, Capital University of Medical Sciences, Beijing 100730, China., Department of Pharmacology, Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093, USA., Departments of Biology and Biochemistry and Molecular Biology, Pennsylvania State University, University Park, PA 16802, USA., Laboratory of Molecular Signaling, Division of Oral Biology and Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA; Eng.A.B Research Chair for Growth Factors and Bone Regeneration, Division of Periodontology, College of Dentistry, King Saud University, Riyadh 11545, Saudi Arabia., Division of Cellular & Molecular Biology, Department of Medical Biophysics, Ontario Cancer Institute, University of Toronto, Toronto, ON M5G 2M9, Canada., Laboratory of Molecular Signaling, Division of Oral Biology and Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: .

Abstract:  Abnormal activation of Wnt/β-catenin-mediated transcription is associated with a variety of human cancers. Here, we report that LATS2 inhibits oncogenic Wnt/β-catenin-mediated transcription by disrupting the β-catenin/BCL9 interaction. LATS2 directly interacts with β-catenin and is present on Wnt target gene promoters. Mechanistically, LATS2 inhibits the interaction between BCL9 and β-catenin and subsequent recruitment of BCL9, independent of LATS2 kinase activity. LATS2 is downregulated and inversely correlated with the levels of Wnt target genes in human colorectal cancers. Moreover, nocodazole, an antimicrotubule drug, potently induces LATS2 to suppress tumor growth in vivo by targeting β-catenin/BCL9. Our results suggest that LATS2 is not only a key tumor suppressor in human cancer but may also be an important target for anticancer therapy. 

Retracted: No

PubPeer comments:
 Figure 5. * Red boxes: The IP:Parafibromin1 b-catenin panels from Figure 5B and Figure 5C look very similar to each other. Could the authors please check or clarify if these are the same experiment? ![file] , 
 Correction, June 2020, found here: https: www.cell.com cell-reports fulltext S2211-1247(20)30772-5?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124720307725%3Fshowall%3Dtrue  In the originally published version of this article, the bottom panel of Figure 5B was inadvertently duplicated with the bottom panel of Figure 5C, due to a mistake during figure assembly. The correct bottom panel of Figure 5B is displayed here. The authors regret this error. ,
Inhibition of PI3Kdelta restores glucocorticoid function in smoking-induced airway inflammation in mice
Authors: Gaetano Caramori
Ian M Adcock
Paolo Casolari
John A Marwick
Christopher S Stevenson
Peter J Barnes
Alberto Papi
Elen Jazrawi
Kazuhiro Ito
Paul A Kirkham
Journal: American Journal of Respiratory and Critical Care Medicine (2009)
Discipline: CLINICAL MEDICINE
Keywords: glucocorticoid therapy; severe asthma; chronic obstructive pulmonary disease; histone deacetylase activity; oxidant stress
Affiliations: Airways Disease Section, National Heart & Lung Institute, Imperial College London, Dovehouse Street, London SW3 6LY, UK. 

Abstract:  Rationale: There is an increasing prevalence of reduced responsiveness to glucocorticoid therapy in severe asthma and chronic obstructive pulmonary disease (COPD). The molecular mechanism of this remains unknown. Recent studies have shown that histone deacetylase activity, which is critical to glucocorticoid function, is altered by oxidant stress and may be involved in the development of glucocorticoid insensitivity. Objectives: To determine the role of phosphoinositol-3-kinase (PI3K) in the development of cigarette smoke-induced glucocorticoid insensitivity. Methods: Wild-type, PI3Kgamma knock-out and PI3Kdelta kinase dead knock-in transgenic mice were used in a model of cigarette smoke-induced glucocorticoid insensitivity. Peripheral lung tissue was obtained from six healthy nonsmokers, nine smokers with normal lung function, and eight patients with COPD. Measurements and main results: In vitro oxidative stress activates PI3K and induced a relative glucocorticoid resistance, which is restored by PI3K inhibition. In vivo, cigarette smoke exposure in mice increased tyrosine nitration of histone deacetylase 2 in the lung, correlating with reduced histone deacetylase 2 activity and reduced glucocorticoid function. Histone deacetylase 2 activity and the antiinflammatory effects of glucocorticoids were restored in PI3Kdelta kinase dead knock-in but not PI3Kgamma knock-out smoke-exposed mice compared with wild type mice, correlating with reduced histone deacetylase 2 tyrosine nitration. Glucocorticoid receptor expression was significantly reduced in smoke-exposed mice, in smokers with normal lung function, and in patients with COPD. Conclusions: These data show that therapeutic inhibition of PI3Kdelta may restore glucocorticoid function in oxidative stress-induced glucocorticoid insensitivity. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
null, 
 #1 I agree with this finding. Unfortunate that the authors are unwilling to correct the scientific record. *** ![file] ,
All-trans retinoic acid restored the osteogenic ability of BMP9 in osteosarcoma through the p38 MAPK pathway
Authors: Nian Wu
Mao Nie
Baicheng He
Qianzhao Chen
Liangjun Yin
Zhongliang Deng
Zijun Meng
Ruidong Li
Journal: International Journal of Oncology (2017)
Discipline: CLINICAL MEDICINE
Keywords: Osteosarcoma; Bone morphogenetic protein 9; BMP9; All-trans retinoic acid; ATRA
Affiliations: Department of Orthopaedics, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, P.R. China., Chongqing Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing Medical University, Chongqing, P.R. China.

Abstract:  Osteosarcoma (OS) is the most common malignant bone tumour and is considered to be a disease caused by a dysfunction in differentiation. Bone morphogenetic protein 9 (BMP9) is the most potent osteogenic factor in mesenchymal stem cells, but it cannot induce osteogenic differentiation in OS cells; this might be one of the determinants in the pathogenesis of OS. All-trans retinoic acid (ATRA) can induce osteogenic differentiation of OS cells and potentiate BMP9-induced osteogenesis in preadipocytes. However, the concomitant effect of ATRA and BMP9 in OS cells is unclear; therefore, in the present study, we focused on this topic. The results showed that BMP9 significantly promoted the proliferation of human OS 143B cells and did not induce osteogenic differentiation of cells in vitro (p&lt;0.01). ATRA inhibited proliferation and induced osteogenesis in 143B cells; these effects could be enhanced by BMP9 overexpression (p&lt;0.05). ATRA could significantly increase the level of phosphorylated p38 MAPK (p-p38) in 143B cells, while BMP9 did not have any significant effect. Notably, BMP9 overexpression enhanced the ability of ATRA to increase the levels of p-p38. Both the osteogenic differentiation and the anti-proliferative activity of BMP9 in the presence of ATRA decreased upon treatment with a specific inhibitor of p38 MAPK (SB203580) (p&lt;0.01). This study indicates that the osteogenic differentiation ability of BMP9 in 143B cells can be restored by ATRA, and the combination of BMP9 and ATRA generated a stronger anti-proliferative effect on 143B cells than ATRA alone. This result may be due to the activation of the p38 MAPK pathway. 

Retracted: No

PubPeer comments:
 Figure 1A: ![file] , 
 The author made a correction. Please check the image. Figure 1A: ![file] ![file] ,
Epigenetic reprogramming and chromatin accessibility in pediatric diffuse intrinsic pontine gliomas: a neural developmental disease
Authors: Stephen Carney
Maria G Castro
Santiago Haase
Felipe J Núñez
Maria B Garcia-Fabiani
Flor M Mendez
Pedro R Lowenstein
Oren J Becher
Jessica C Gauss
Journal: Neuro-oncology (2020)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: DIPG; H3 K27M; epigenetics; histone variants.
Affiliations: Department of Cell and Developmental Biology and Department of Neurosurgery, University of Michigan Medical School, Ann Arbor, Michigan., Department of Pediatrics, Northwestern University, Chicago, Illinois., Ann & Robert Lurie Children's Hospital of Chicago, Division of Hematology-Oncology and Stem Cell Transplant, Chicago, Illinois.

Abstract:  Diffuse intrinsic pontine glioma (DIPG) is a rare but deadly pediatric brainstem tumor. To date, there is no effective therapy for DIPG. Transcriptomic analyses have revealed DIPGs have a distinct profile from other pediatric high-grade gliomas occurring in the cerebral hemispheres. These unique genomic characteristics coupled with the younger median age group suggest that DIPG has a developmental origin. The most frequent mutation in DIPG is a lysine to methionine (K27M) mutation that occurs on H3F3A and HIST1H3B/C, genes encoding histone variants. The K27M mutation disrupts methylation by polycomb repressive complex 2 on histone H3 at lysine 27, leading to global hypomethylation. Histone 3 lysine 27 trimethylation is an important developmental regulator controlling gene expression. This review discusses the developmental and epigenetic mechanisms driving disease progression in DIPG, as well as the profound therapeutic implications of epigenetic programming. 

Retracted: No

PubPeer comments:
 This is a very helpful review, but there are mistakes in the citations, starting somewhere with citation 20 21. Reference #20 is never used in the paper s text, and somehow the numbering of all the other references in the text was thrown off, and references are cited in places where they don t belong. For example  Survival and apoptosis in the developing and adult nervous systems are regulated by p53. 30 links to a paper about ACVR1. Because many references are cited multiple times, it is very difficult to figure out which reference is applicable. Can the authors fix this? , 
 #1 Thanks for bringing this to my attention. I will look into it and get back to you soon. ,
Biosynthesis of silver nanoparticles using Acacia leucophloea extract and their antibacterial activity
Authors: Saleh Al-Sohaibani
Balakrishnan Senthilkumar
Kasi Murugan
Duraisamy Senbagam
Journal: International journal of nanomedicine (2014)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Acacia leucophloea; AgNPs; FTIR; TEM; XRD
Affiliations: Department of Microbiology and Botany, College of Science, King Saud University, Riyadh, Saudi Arabia.

Abstract:  The immense potential of nanobiotechnology makes it an intensely researched field in modern medicine. Green nanomaterial synthesis techniques for medicinal applications are desired because of their biocompatibility and lack of toxic byproducts. We report the toxic byproducts free phytosynthesis of stable silver nanoparticles (AgNPs) using the bark extract of the traditional medicinal plant Acacia leucophloea (Fabaceae). Visual observation, ultraviolet-visible spectroscopy, and transmission electron microscopy (TEM) were used to characterize the synthesized AgNPs. The visible yellow-brown color formation and surface plasmon resonance at 440 nm indicates the biosynthesis of AgNP. The TEM images show polydisperse, mostly spherical AgNP particles of 17-29 nm. Fourier transform infrared spectroscopy revealed that primary amines, aldehyde/ketone, aromatic, azo, and nitro compounds of the A. leucophloea extract may participate in the bioreduction and capping of the formed AgNPs. X-ray diffraction confirmed the crystallinity of the AgNPs. The in vitro agar well diffusion method confirmed the potential antibacterial activity of the plant extract and synthesized AgNPs against the common bacterial pathogens Staphylococcus aureus (MTCC 737), Bacillus cereus (MTCC 1272), Listeria monocytogenes (MTCC 657), and Shigella flexneri (MTCC 1475). This research combines the inherent antimicrobial activity of silver metals with the A. leucophloea extract, yielding antibacterial activity-enhanced AgNPs. This new biomimetic approach using traditional medicinal plant (A. leucophloea) barks to synthesize biocompatible antibacterial AgNPs could easily be scaled up for additional biomedical applications. These polydisperse AgNPs green-synthesized via A. leucophloea bark extract can readily be used in many applications not requiring high uniformity in particle size or shape. 

Retracted: No

PubPeer comments:
 Figure 5 legend: u201cStaphylococcus aureus (A), Bacillus cereus (B)u201d https: imgur.com a NaJUzuQ ,
miR‐206 inhibits thyroid cancer proliferation and invasion by targeting RAP1B
Authors: Jialei Gu
Jinbiao Shang
Kejing Wang
Peng Wang
Wendong Wang
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: RAP1B; invasion; miR-206; proliferation; thyroid cancer.
Affiliations: Department of Head and Neck SurgeryInstitute of Cancer Research and Basic Medical Sciences of Chinese Academy of Sciences, Cancer Hospital of University of Chinese Academy of Sciences, Zhejiang Cancer Hospital Zhejiang China

Abstract:  Thyroid cancer (TC) is one of the primary tumors arisen from endocrine system. The purpose of this study was to investigate the underlying mechanism by which RAP1B (Ras-related protein Rap-1b) modulates microRNA (miR)-206 related effects on TC cells. Expression of miR-206 and RAP1B was analyzed in cells and tissues. miR-206 mimics or inhibitors and RAP1B vector were used in functional experiments to investigate the effects of miR-206 and RAP1B on cell activities including proliferation, migration, and invasion. Luciferase assay was performed to explore the association between miR-206 and RAP1B. The influence of miR-206 on tumorigenesis of TC cells was investigated using an ex vivo model. Our results demonstrated the reduce of miR-206 in TC tissues and cell lines in which RAP1B was increased. Overexpression of miR-206 significantly inhibited the functional capacities of TPC-1 cells including proliferation, invasion, and migration, most likely, through reducing the expression of RAP1B. Xenograft experiment showed that increased miR-206 could effectively inhibit the tumorigenesis of TC cells. Our study showed that miR-206 negatively regulated cell activities of proliferation, invasion, and migration in TC via suppressing RAP1B expression, suggesting that miR-206 exerts a vital role in TC. 

Retracted: No

PubPeer comments:
 In Figure 4D, microscopy data has been duplicated and presented as something else. ![file] ,
Targeting the eIF4A RNA helicase blocks translation of the MUC1-C oncoprotein
Authors: D Kufe
C M Rodrigo
J A Porco Jr
H Rajabi
C Jin
Journal: Oncogene (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MUC1-C; breast cancer; growth factor; translation; PI3K/AKT
Affiliations: Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA, USA.

Abstract:  The oncogenic MUC1 C-terminal subunit (MUC1-C) subunit is aberrantly overexpressed in most human breast cancers by mechanisms that are not well understood. The present studies demonstrate that stimulation of non-malignant MCF-10A cells with epidermal growth factor (EGF) or heregulin (HRG) results in marked upregulation of MUC1-C translation. Growth factor-induced MUC1-C translation was found to be mediated by PI3KAKT, and not by MEKERK1/2, signaling. We also show that activation of the mammalian target of rapamycin complex 1 (mTORC1)ribosomal protein S6 kinase 1 (S6K1) pathway decreases tumor suppressor programmed cell death protein 4 (PDCD4), an inhibitor of the eIF4A RNA helicase, and contributes to the induction of MUC1-C translation. In concert with these results, treatment of growth factor-stimulated MCF-10A cells with the eIF4A RNA helicase inhibitors, silvestrol and CR-1-31-B, blocked increases in MUC1-C abundance. The functional significance of the increase in MUC1-C translation is supported by the demonstration that MUC1-C, in turn, forms complexes with EGF receptor (EGFR) and promotes EGFR-mediated activation of the PI3KAKT pathway and the induction of growth. Compared with MCF-10A cells, constitutive overexpression of MUC1-C in breast cancer cells was unaffected by EGF stimulation, but was blocked by inhibiting PI3KAKT signaling. The overexpression of MUC1-C in breast cancer cells was also inhibited by blocking eIF4A RNA helicase activity with silvestrol and CR-1-31-B. These findings indicate that EGF-induced MUC1-C expression is mediated by the PI3KAKT pathway and the eIF4A RNA helicase, and that this response promotes EGFR signaling in an autoinductive loop. The findings also indicate that targeting the eIF4A RNA helicase is a novel approach for blocking MUC1-C overexpression in breast cancer cells. 

Retracted: No

PubPeer comments:
 Figure 6c much more similar than expected. ![file] ,
hsa-miR-520h downregulates ABCG2 in pancreatic cancer cells to inhibit migration, invasion, and side populations
Authors: Z Xu
J Wu
Y Miao
X Xue
C Dai
J Wei
F Wang
H Cai
J Yao
Z Qian
Y An
Journal: British journal of cancer (2010)
Discipline: CLINICAL MEDICINE
Keywords: ABCG2; miRNA; pancreatic cancer; hsa-miR-520h; gene therapy
Affiliations: Laboratory of General Surgery, First Affiliated Hospital of Nanjing Medical University, Nanjing 210009, PR China.

Abstract:  Background: Expression of ABCG2 is normally absent or low in the pancreas, but high in human pancreatic cancer cells. The mechanism by which ABCG2 is altered in human cancers remains unknown. Methods: We investigated ABCG2 expression in four pancreatic cancer cell lines, and used three microRNA (miRNA) target prediction programmes, and information from the existing literature to predict and identify hsa-miR-520h as an miRNA that targets ABCG2. The function of this miRNA was investigated by transient transfection of the pancreatic cancer cell line PANC-1 with oligonucleotides that mimic hsa-miR-520h. Results: Results showed that both mRNA and protein levels of ABCG2 were reduced, indicating that it was a target of hsa-miR-520h. Introduction of hsa-miR-520h mimics into PANC-1 cells also resulted in inhibition of cell migration and invasion, and reduction of side population cells. Cell proliferation, cell cycle progression and apoptosis were not affected. Conclusions: We propose that the effects of hsa-miR-520h may be, at least in part, caused by its regulation of ABCG2. Thus, our findings provide a new insight into the function of miRNA in the regulation of ABCG2 expression in pancreatic cancer. Gene therapy using miRNA mimics may therefore be useful as a pancreatic cancer therapy. 

Retracted: No

PubPeer comments:
 unexpected image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
EGFR activation and signaling in cancer cells are enhanced by the membrane-bound metalloprotease MT4-MMP
Authors: Agnès Noel
Nor Eddine Sounni
Guy Jerusalem
Jean Michel Foidart
Didier Cataldo
Joelle Collignon
Philippe Delvenne
Silvia Blacher
Cassandre Yip
Alice Truong
Carine Munaut
Erik Maquoi
Jonathan Cimino
Alexandra Paye
Journal: Cancer Research (2014)
Discipline: CLINICAL MEDICINE
Keywords: MT4-MMP; cancer cell proliferation; EGFR; metastasis; CDK4 activation
Affiliations: Laboratory of Tumor and Developmental Biology, Groupe Interdisciplinaire de Génoprotéomique Appliquée-Cancer (GIGA-Cancer), University of Liège, Liège, Belgium., Department of Medical Oncology, Centre Hospitalier Universitaire (CHU), Sart Tilman, Liège, Belgium., Department of Pathology, University of Liège, Liège, Belgium., Laboratory of Tumor and Developmental Biology, Groupe Interdisciplinaire de Génoprotéomique Appliquée-Cancer (GIGA-Cancer), University of Liège, Liège, Belgium.  .

Abstract:  MT4-MMP (MMP-17) is a glycosylphosphatidyl inositol-anchored matrix metalloprotease expressed on the surface of cancer cells that promotes tumor growth and metastasis. In this report, we identify MT4-MMP as an important driver of cancer cell proliferation through CDK4 activation and retinoblastoma protein inactivation. We also determine a functional link between MT4-MMP and the growth factor receptor EGFR. Mechanistic experiments revealed direct association of MT4-MMP and its positive effects on EGFR phosphorylation in response to TGFα and EGF in cancer cells. Notably, the effects of MT4-MMP on proliferation and EGFR activation did not rely on metalloprotease activity. Clinically, MT4-MMP and EGFR expressions were correlated in human triple-negative breast cancer specimens. Altogether, our results identify MT4-MMP as a positive modifier of EGFR outside-in signaling that acts to cooperatively drive cancer cell proliferation. 

Retracted: No

PubPeer comments:
 Figure 6C. Much more similar and different than expected. ![file] , 
 2022 Editor s Note. https: aacrjournals.org cancerres article-abstract 82 4 734 678081 Editor-s-Note-EGFR-Activation-and-Signaling-in?redirectedFrom=fulltext The editors are publishing this note to alert readers to concerns about this article (1). In Fig. 2, the actin loading control bands for cyclin D1 and cyclin D2 are identicalu2013the authors clarified that the Western blots for cyclin D1 and cyclin D2 were performed on the same samples, however, this was not indicated in the figure legend. Additionally, in Fig. 6C, the p-EGFR bands in MDA-MB-231 cells showing stimulation by TGFu03b1 treatment are identical to the p-EGFR bands showing stimulation by EGF treatment. In the original submission of this manuscript, a correct version of this figure was used to show both TGFu03b1 and EGF could stimulate p-EGFR in control vector (CTR)u2013 and MT4-MMPu2013expressing (MT4) MDA-MB-231 cells, but these panels were mistakenly duplicated in the revised and final versions of the manuscript. ,
iGPCR-drug: a web server for predicting interaction between GPCRs and drugs in cellular networking
Authors: Jian-Liang Min
Xuan Xiao
Kuo-Chen Chou
Pu Wang
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: G-protein-coupled receptors (GPCRs); therapeutic drugs; computational methods; 3D structure; iGPCR-drug
Affiliations: Computer Department, Jing-De-Zhen Ceramic Institute, Jing-De-Zhen, China ; Information School, ZheJiang Textile and Fashion College, NingBo, China ; Gordon Life Science Institute, Belmont, Massachusetts, United States of America.

Abstract:  Involved in many diseases such as cancer, diabetes, neurodegenerative, inflammatory and respiratory disorders, G-protein-coupled receptors (GPCRs) are among the most frequent targets of therapeutic drugs. It is time-consuming and expensive to determine whether a drug and a GPCR are to interact with each other in a cellular network purely by means of experimental techniques. Although some computational methods were developed in this regard based on the knowledge of the 3D (dimensional) structure of protein, unfortunately their usage is quite limited because the 3D structures for most GPCRs are still unknown. To overcome the situation, a sequence-based classifier, called "iGPCR-drug", was developed to predict the interactions between GPCRs and drugs in cellular networking. In the predictor, the drug compound is formulated by a 2D (dimensional) fingerprint via a 256D vector, GPCR by the PseAAC (pseudo amino acid composition) generated with the grey model theory, and the prediction engine is operated by the fuzzy K-nearest neighbour algorithm. Moreover, a user-friendly web-server for iGPCR-drug was established at http://www.jci-bioinfo.cn/iGPCR-Drug/. For the convenience of most experimental scientists, a step-by-step guide is provided on how to use the web-server to get the desired results without the need to follow the complicated math equations presented in this paper just for its integrity. The overall success rate achieved by iGPCR-drug via the jackknife test was 85.5%, which is remarkably higher than the rate by the existing peer method developed in 2010 although no web server was ever established for it. It is anticipated that iGPCR-Drug may become a useful high throughput tool for both basic research and drug development, and that the approach presented here can also be extended to study other drug - target interaction networks. 

Retracted: No

PubPeer comments:
 This paper is extremely similar to https: doi.org 10.1155 2013 701317 ,
Curcumin loaded polycaprolactone-/polyvinyl alcohol-silk fibroin based electrospun nanofibrous mat for rapid healing of diabetic wound: An in-vitro and in-vivo studies
Authors: Sneha Anand
Prashant Pandey
Dilip Kumar Arya
Upama Tiwari
Shivendu Ranjan
J Balasubramnaiam
Yashi Agarwal
P S Rajinikanth
Payal Deepak
Journal: International Journal of Biological Macromolecules (2021)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Polycaprolactone (PCL); Polyvinyl alcohol (PVA); Silk fibroin.
Affiliations: Department of Pharmaceutical Sciences, Babasaheb Bhimrao Ambedkar University, Lucknow, India., Department of Pharmaceutical Sciences, Babasaheb Bhimrao Ambedkar University, Lucknow, India. Electronic address: ., Faculty of Engineering and the Built Environment, University of Johannesburg, Johannesburg, South Africa. Electronic address: ., Environ Care Products LLP, Greater Noida, India., Research and Development Centre, Epion Labs Pvt Ltd., Hyderabad, India.

Abstract:  Electrospinning is emerging as a versatile technique nanofibers fabrication because due to their unique properties such as large surface area to volume ratio, porosity and maintaining moist wound environment, the nanofibers are able to deliver sustained drug release and oxygen to the wound for rapid healing of diabetic wound. The present work was aimed to prepare and evaluate silk fibroin-curcumin based nanofiber in combination with polycaprolactone (PCL) and polyvinyl alcohol (PVA) which helped to strengthen the wound healing properties of nanofiber. Silk fibroin is a naturally occurring polymer was selected one polymer for making nanofibrous mat due to its unique properties such as biodegradability, permeability, oxygen supply and maintain moisture content in the wound. SEM results showed diameters of fibers varied in the range between 200 and 350 nm and their tensile strength ranged from 12.41 to 16.80 MP. The nanofibers were causing sustained release of curcumin for many hours. The in-vivo wound healing studies in streptozotocin-induced diabetic mice showed rapid wound healing efficacy as compared to conventional formulations. Furthermore, the histopathological studies evidenced its ability to restore the normal skin structure and histological conditions of tissues. The silk fibroin-based nanofiber wound dressing, therefore appears to be an ideal preparation, in combination with curcumin, because it blends the anti-oxidant, anti-inflammatory properties of curcumin. Therefore, it was concluded that the silk fibroin-based nanofiber loaded with curcumin has great healing potential in diabetic wound. 

Retracted: No

PubPeer comments:
 Figure 8: There is a photo duplication in the control group, I ve added some red boxes and a connecting line to show where I mean. The colouring is slightly different, as is the cropping. Would the authors comment? ![file] ,
A correlation between altered O-GlcNAcylation, migration and with changes in E-cadherin levels in ovarian cancer cells
Authors: De-zhang Zhao
Chao Yu
Feng-zhen Jin
Zhu Yang
Ming-jun Wu
Journal: Experimental Cell Research (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: O-GlcNAcylation; posttranslational modification; ovarian cancer cells; migration; metastasis

Abstract:  O-GlcNAcylation is a dynamic and reversible posttranslational modification of nuclear and cytoplasmic proteins. In recent years, the roles of O-GlcNAcylation in several human malignant tumors have been investigated, and O-GlcNAcylation was found to be linked to cellular features relevant to metastasis. In this study, we modeled four diverse ovarian cancer cells and investigated the effects of O-GlcNAcylation on ovarian cancer cell migration. We found that total O-GlcNAcylation level was elevated in HO-8910PM cells compared to OVCAR3 cells. Additionally, through altering the total O-GlcNAcylation level by OGT silencing or OGA inhibition, we found that the migration of OVCAR3 cells was dramatically enhanced by PUGNAc and Thiamet G treatment, and the migration ability of HO-8910PM cells was significantly inhibited by OGT silencing. Furthermore, we also found that the expression of E-cadherin, an O-GlcNAcylated protein in ovarian cancer cells, was reduced by OGA inhibition in OVCAR3 cells and elevated by OGT silencing in HO-8910PM cells. These results indicate that O-GlcNAcylation could enhance ovarian cancer cell migration and decrease the expression of E-cadherin. Our studies also suggest that O-GlcNAcylation might become another potential target for the therapy of ovarian cancer. 

Retracted: No

PubPeer comments:
 ![file] ![file] , 
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