PReD-Bench/PRed-Bench huggingface dataset:
Reef ecology. Chemically mediated behavior of recruiting corals and fishes: a tipping point that may limit reef recovery
Authors: David Abrego
Danielle L Dixson
Mark E Hay
Journal: Science (2014)
Discipline: Multidisciplinary
Keywords: Coral reefs; seaweed dominance; herbivores; coral recovery; fish recruitment
Affiliations: School of Biology, Georgia Institute of Technology, 310 Ferst Drive, Atlanta, GA 30332, USA., Department of Natural Sciences and Public Health, Zayed University, Abu Dhabi, United Arab Emirates., School of Biology, Georgia Institute of Technology, 310 Ferst Drive, Atlanta, GA 30332, USA. .

Abstract:  Coral reefs are in global decline, converting from dominance by coral to dominance by seaweed. Once seaweeds become abundant, coral recovery is suppressed unless herbivores return to remove seaweeds, and corals then recruit. Variance in the recovery of fishes and corals is not well understood. We show that juveniles of both corals and fishes are repelled by chemical cues from fished, seaweed-dominated reefs but attracted to cues from coral-dominated areas where fishing is prohibited. Chemical cues of specific seaweeds from degraded reefs repulsed recruits, and cues from specific corals that are typical of healthy reefs attracted recruits. Juveniles were present at but behaviorally avoided recruiting to degraded reefs dominated by seaweeds. For recovery, degraded reefs may need to be managed to produce cues that attract, rather than repel, recruiting corals and fishes. 

Retracted: No

PubPeer comments:
 See https: steamtraen.blogspot.com 2021 05 todays-topic-is-report-xxlink-in.html for a blogpost and a report about concerns with the dataset of this article. See also https: www.sciencemag.org news 2021 05 does-ocean-acidification-alter-fish-behavior-fraud-allegations-create-sea-doubt , 
 February 17, 2022 u201cOn 22 August 2014, Science published the Research Article u201cChemically mediated behavior of recruiting corals and fishes: A tipping point that may limit reef recoveryu201d by D. L. Dixson et al. (1). Science has been made aware of data manipulation accusations pertaining to this paper. We are publishing this Editorial Expression of Concern to make readers aware of these accusations while the lead authoru2019s current and postdoctoral institutions investigate the claims.u201d https: www.science.org doi 10.1126 science.abo1771 See also: https: retractionwatch.com 2022 02 17 science-issues-expression-of-concern-nine-months-after-its-reporter-uncovers-potential-misconduct , 
 Retracted: https: www.science.org doi 10.1126 science.ade2691 , 
 Nick has an update too. https: steamtraen.blogspot.com 2022 08 an-interesting-lack-of-randomness-in.html , 
 More backgrounds at https: www.science.org content article star-marine-ecologist-committed-misconduct-university-says ,
PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma
Authors: Hui Cong
Xudong Wang
Qingqing Yin
Shaoqing Ju
Xianjuan Shen
Shan Kong
Qian Yang
Journal: Journal of Cellular and Molecular Medicine (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MAP3K7; NF-κB; lncRNA; miRNA; multiple myeloma.
Affiliations: Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, China., Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China.

Abstract:  Loss of one or some specific miRNA-mediated regulation is closely associated with malignant progression of multiple myeloma (MM). But how these miRNAs work and what role the specific miRNA plays in this process of malignant progression remain unclear. It was found in this study that the expression of miR-129 was decreased in both MM cell lines and newly diagnosed MM patients. Further clinicopathological statistics showed that miR-129 was correlated with the isotype of MM patients. MiR-129 overexpression disturbed cell proliferation, cell cycle evolution and spurred apoptosis both in vitro and in vivo. MAP3K7, a kinase able to activate NF-κB circuit, was found to be up-regulated in MM and contain a binding target of miR-129. In addition, lncRNA PCAT-1 functioned to sponge miR-129 and thereby lowered its expression. PCAT-1 knockdown eliminated the tumour-promoting effect caused by miR-129 inhibition, probably through repressing MAP3K7 and subsequent NF-κB activation. To the best of our knowledge, this is the first study to have discovered that increased expression of PCAT-1 could augment cell proliferation and cycle procession and inhibit apoptosis by down-regulating miR-129 via the MAP3K7/NF-κB pathway in MM. 

Retracted: No

PubPeer comments:
 Retracted. backgrounds at https: retractionwatch.com 2020 02 12 journals-retract-three-papers-by-hans-eysenck-flag-18-some-60-years-old ,
Mechanisms of OGT2115 inhibition of invasion and migration in KB oral cancer cells
Authors: J-X Tang
S Shen
Journal: European review for medical and pharmacological sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: OGT2115; inhibition; invasion; migration; KB oral cancer cells
Affiliations: Department of Stomatology, The First Affiliated Hospital of Jinan University, Guangzhou, China.

Abstract:  The article "Mechanisms of OGT2115 inhibition of invasion and migration in KB oral cancer cells" by S. Shen, J.-X. Tang, published in Eur Rev Med Pharmacol Sci 2017; 21 (1): 55-60 has been withdrawn. 

Retracted: No

PubPeer comments:
 This article has been retracted ,
Knockdown survivin expression reduces the efficacy of curcumin treatment in hepatocellular carcinoma cells
Authors: Chien-Ming Chen
Po-Li Wei
Hui-Hsiung Liu
Yuan-Soon Ho
Chin-Sheng Hung
Li-Jen Kuo
Yu-Jia Chang
Ming-Te Huang
Chao-Wen Cheng
Chih-Hsiung Wu
Journal: Annals of surgical oncology (2012)
Discipline: CLINICAL MEDICINE
Keywords: Survivin; curcumin treatment; hepatocellular carcinoma; therapeutic resistance; short interfering RNA
Affiliations: Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Abstract:  Background: Survivin is a potential therapeutic target for cancer. Increased survivin expression promotes cell survival and therapeutic resistance. However, there is little information regarding whether the expression level of survivin affects curcumin treatment in hepatocellular carcinoma (HCC). Methods: Survivin expression was suppressed in HCC cells using a short interfering RNA (siRNA) technique. The anticancer effects of curcumin were examined using a biosensor system, MTT assay, TUNEL assay, and cell cycle analysis. Results: Curcumin resistance developed in cells with suppressed survivin, in contrast to the parental cells, as determined by survival assays. Cell cycle analysis and TUNEL assays revealed that the apoptotic cell population was increased in the scrambled-siRNA cells treated with curcumin compared with the survivin-siRNA cells. Suppression of survivin expression resulted in curcumin resistance via the modulation of Bcl-2 and Bax expression. Conclusions: We conclude that the expression levels of survivin may mediate the therapeutic efficacy of curcumin in HCC cells. 

Retracted: No

PubPeer comments:
 Identified by another reader. Other paper: https: pubpeer.com publications 76E03678885F39B46D2A9D0AB33C7D#2 *** ![file] ,
Full activation of PKB/Akt in response to insulin or ionizing radiation is mediated through ATM
Authors: José María Rojas
Pegah Modirassari
Carlos Parada Cobo
Javier Hernández Losa
Víctor Javier Sánchez-Arévalo Lobo
Luis Alvarez-Vallina
Natalia Martínez
Ricardo Sánchez-Prieto
Clara Isabel Aceves Luquero
Santiago Ramón y Cajal
Juan Guinea Viniegra
Journal: Journal of Biological Chemistry (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ATM; PKB/Akt; cell cycle control; DNA damage; insulin
Affiliations: CRIB/Facultad de Medicina, Universidad de Castilla la Mancha, 02071 Albacete, Spain.

Abstract:  The gene mutated in ataxia telangiectasia, ATM, has been implicated in several cell functions such as cell cycle control and response to DNA damage and insulin. PKB/Akt has also been implicated in the cellular response to insulin, gamma-radiation, and cell cycle control. Interestingly, lack of PKB/Akt function in vivo is able to mimic some phenotypic abnormalities associated with ataxia telangiectasia (AT). Here we show that ATM is a major determinant of full PKB/Akt activation in response to insulin or gamma-radiation. This effect is mediated through the phosphatidylinositol 3-kinase domain of ATM that specifically affects Akt serine 473 phosphorylation. This conclusion was inferred from the results obtained in transient transfection assays using exogenous PKB/Akt and ATM in Cos cells. Moreover, the use of ATM inhibitors or small interfering RNA confirmed our observation. Further supporting these results, we also observed that biological responses tightly regulated by Akt, such as transcription factor of the forkhead family activity after insulin treatment or gamma-radiation response, were altered in cell lines derived from AT patients and knockout mice for ATM in which phosphorylation in serine 473 was almost abolished. This study proposes new clues in the search of the unknown PDK2 and new explanations for the radiosensitivity or insulin intolerance described more than 30 years ago in AT patients. 

Retracted: No

PubPeer comments:
 ![file] , 
 #1 I tentatively agree with this concern. It would be very helpful if the authors could provide an original or higher resolution image. ![file] ,
Long Noncoding RNA NEAT1 Promotes Proliferation and Invasion via Targeting miR-181a-5p in Non-Small Cell Lung Cancer
Authors: Yubing Xia
Kun-Peng Yang
JiaMei Yang
ShiDong Li
QingXia Fan
Journal: Oncology research (2018)
Discipline: CLINICAL MEDICINE
Keywords: lncRNAs; NEAT1; non-small cell lung cancer; tumorigenesis; TNM stages
Affiliations: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R. China., Department of Oncology, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R. China., Department of Radiotherapy, Kaifeng Cancer Hospital, Kaifeng, P.R. China., Department of Thoracic Surgery, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R. China.

Abstract:  Long noncoding RNAs (lncRNAs) have been implicated in various biological processes and pathological conditions, including tumorigenesis. However, the exact roles of NEAT1 and its underlying mechanisms in non-small cell lung cancer (NSCLC) remain largely unclear. In the present study, lncRNA NEAT1 was detected to be significantly upregulated in NSCLC tissues and closely associated with advanced TNM stages, lymph node metastasis, distant metastasis, and poor prognosis. Further experiments revealed that lncRNA NEAT1 silencing inhibited cell proliferation and invasion in vitro. In addition, mechanistic analysis showed that lncRNA NEAT1 upregulated the miR-181a-5p-targeted gene HMGB2 through acting as a competitive "sponge" of miR-181a-5p. In conclusion, our study suggested that lncRNA NEAT1 plays an oncogenic role in NSCLC progression and provides potential mechanisms by which lncRNA NEAT1 contributes to this disease. 

Retracted: No

PubPeer comments:
 Retraction - [11 January 2021] ----------------------------------------------------------- We, the Editors and Publisher of the journal Artificial Cells, Nanomedicine, and Biotechnology, have retracted the following article: Zhiguo Yang, Dongyan Liu, Dan Wu, Fang Liu Cuiping Liu (2019) The biological function of long noncoding RNA FAL1 in oesophageal carcinoma cells. Artificial Cells, Nanomedicine, and Biotechnology, 47:1, 896u2013903, DOI: 10.1080 21691401.2019.1573738 It has come to our attention that the full authorship list and affiliations for this manuscript, including the study site and ethics committee, were changed after the article was submitted. We have contacted the corresponding author for an explanation, but we have not received a satisfactory explanation. As determining authorship and the location of where the research was conducted is core to the integrity of published work, we are therefore retracting the article. The corresponding author listed in this publication has been informed. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u2018Retractedu2019. ,
Three redundant murein endopeptidases catalyse an essential cleavage step in peptidoglycan synthesis of Escherichia coli K12
Authors: Manjula Reddy
Santosh Kumar Singh
Ravi N Amrutha
L SaiSree
Journal: Molecular microbiology (2012)
Discipline: MICROBIOLOGY
Keywords: Bacterial peptidoglycan; murein; cleavage; enzymes; Escherichia coli
Affiliations: Centre for Cellular and Molecular Biology, Hyderabad 500007, India.

Abstract:  Bacterial peptidoglycan (PG or murein) is a single, large, covalently cross-linked macromolecule and forms a mesh-like sacculus that completely encases the cytoplasmic membrane. Hence, growth of a bacterial cell is intimately coupled to expansion of murein sacculus and requires cleavage of pre-existing cross-links for incorporation of new murein material. Although, conceptualized nearly five decades ago, the mechanism of such essential murein cleavage activity has not been studied so far. Here, we identify three new murein hydrolytic enzymes in Escherichia coli, two (Spr and YdhO) belonging to the NlpC/P60 peptidase superfamily and the third (YebA) to the lysostaphin family of proteins that cleave peptide cross-bridges between glycan chains. We show that these hydrolases are redundantly essential for bacterial growth and viability as a conditional mutant lacking all the three enzymes is unable to incorporate new murein and undergoes rapid lysis upon shift to restrictive conditions. Our results indicate the step of cross-link cleavage as essential for enlargement of the murein sacculus, rendering it a novel target for development of antibacterial therapeutic agents. 

Retracted: No

PubPeer comments:
 ![file] , 
 Thanks for the observation. As pointed out, the same chromatogram is used in both Fig. 2D and Fig. 4C because that image represents a control sample in which the substrate (Tetra-Tetra) is incubated with buffer alone whereas Figs. 2E, 4E and 4F represent samples in which the enzymes, Spr, YdhO and YebA have been added, respectively. This is due to setting up all the four reactions at the same time; hence they have one common control. As the data was split into two figures, both have the same control chromatogram. ,
Small interfering RNA targeting heme oxygenase-1 enhances ischemia-reperfusion-induced lung apoptosis
Authors: Paul W Noble
Peiying Shan
Patty J Lee
Xuchen Zhang
Dianhua Jiang
Attallah Kappas
Nader G Abraham
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Heme oxygenase-1; cytoprotective enzyme; injury models; therapeutic applications; mechanisms
Affiliations: Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8057, USA.

Abstract:  Heme oxygenase-1 (HO-1) is emerging as an important cytoprotective enzyme system in a variety of injury models. To optimize future therapeutic applications of HO-1, it is necessary to delineate the precise functions and mechanisms as well as modes of externally regulating HO-1 expression. Investigations have been limited by difficulties with the generation of HO-1 null mice and the lack of specific HO-1 inhibitors. Lung ischemia-reperfusion (I-R) injury is the inciting event in acute lung failure following transplantation, surgery, and shock. To study the function of HO-1 in I-R-induced lung injury, we designed small interfering RNA (siRNA) sequences that effectively suppress HO-1 expression both in vitro and in vivo in an organ-specific manner. In this study we show that there is enhanced apoptosis, via increased Fas expression and caspase 3 activity, in the presence of HO-1 siRNA in endothelial cells and mouse lung during I-R injury, whereas HO-1 overexpression attenuates apoptosis. To the best of our knowledge, we are the first to demonstrate that lung-specific siRNA delivery can be achieved by intranasal administration without the need for viral vectors or transfection agents in vivo, thereby obviating potential concerns for toxicity if siRNA technology is to have clinical application in the future. 

Retracted: No

PubPeer comments:
 Figure 2B. Heart HO-1 and beta-tubulin panels not from same blot. https: imgur.com 65tf7BQ , 
 #1 It just seems to be that one is vertically inverted. , 
 #2 I thought that at first, but if you do that they still do not look they come from the same blot. The HO-1 and beta-tubulin panels from the other organs align much better. https: imgur.com UPotWAS ,
Mutations in the helix 3 region of the androgen receptor abrogate ARA70 promotion of 17beta-estradiol-induced androgen receptor transactivation
Authors: Tin Htwe Thin
Chawnshang Chang
Loretta L Collins
Erik R Sampson
Ravi Basavappa
Shuyuan Yeh
Eungseok Kim
Yei-Tsung Chen
Journal: Journal of Biological Chemistry (2002)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: estrogen; male reproductive system; partial androgen insensitivity syndrome (PAIS); androgen receptor (AR); steroid metabolism enzymes
Affiliations: George Whipple Laboratory for Cancer Research, Department of Pathology, University of Rochester, Rochester, New York 14642, USA.

Abstract:  The influence of estrogen on the development of the male reproductive system may be interrupted in a subset of partial androgen insensitivity syndrome (PAIS) patients. PAIS describes a wide range of male undermasculinization resulting from mutations in the androgen receptor (AR) or steroid metabolism enzymes that perturb androgen-AR regulation of male sex organ development. In this study, we are interested in determining if PAIS-derived AR mutants that respond normally to androgen have altered responses to estrogen in the presence of ARA70, a coregulator previously shown to enhance 17beta-estradiol E2-induced AR transactivation. The wild-type AR (wtAR) and two PAIS AR mutants, AR(S703G) and AR(E709K), all bind to androgen and E2 and subsequently translocate to the nucleus. Whereas ARA70 functionally interacts with the wtAR and the PAIS AR mutants in response to androgen, E2 only promotes the functional interaction between ARA70 and the wtAR but not the PAIS AR mutants. ARA70 increases E2 competitive binding to the wtAR in the presence of low level androgen and also retards E2 dissociation from the wtAR. ARA70 is present in both the cytoplasm and the nucleus of various mouse testicular cells during early embryogenesis day 16, at postpartum day 0 during estradiol synthesis and in the Leydig cells at postpartum day 49. ARA70 may be unable to modulate the PAIS AR mutants-E2 binding, diminishing the effect of E2 via AR during male reproductive system development in patients with such mutations. Therefore, the presence of ARA70 in the testosterone and E2-producing Leydig cells may enhance the overall activity of AR during critical stages of male sex organ development. 

Retracted: No

PubPeer comments:
 there is a peculiar undeclared horizontal discontinuity in Figure 4A. Looks like the AR top was spliced onto the ARA70 bottom. I marked splice with blue arrow ![file] ,
TGF-β1 regulation of estrogen production in mature rat Leydig cells
Authors: Zong-Ren Wang
Jing Ma
Yan-Qiu Chen
Huan Wang
Man-Li Liu
Yuan-Qiang Zhang
Yu-Fen Zhang
Zhen Li
Fang-Hong Zhu
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Leydig cells; TGF-β1; estradiol; Cx43; gap junctional intercellular communication
Affiliations: Department of Traditional Chinese Medicine, Xijing Hospital, the Fourth Military Medical University, Xi'an, People's Republic of China.

Abstract:  Background: Besides androgens, estrogens produced in Leydig cells are also crucial for mammalian germ cell differentiation. Transforming growth factor-β1 (TGF-β1) is now known to have multiple effects on regulation of Leydig cell function. The objective of the present study is to determine whether TGF-β1 regulates estradiol (E2) synthesis in adult rat Leydig cells and then to assess the impact of TGF-β1 on Cx43-based gap junctional intercellular communication (GJIC) between Leydig cells. Methodology/principal findings: Primary cultured Leydig cells were incubated in the presence of recombinant TGF-β1 and the production of E2 as well as testosterone (T) were measured by RIA. The activity of P450arom was addressed by the tritiated water release assay and the expression of Cyp19 gene was evaluated by Western blotting and real time RT-PCR. The expression of Cx43 and GJIC were investigated with immunofluorescence and fluorescence recovery after photo-bleaching (FRAP), respectively. Results from this study show that TGF-β1 down-regulates the level of E2 secretion and the activity of P450arom in a dose-dependent manner in adult Leydig cells. In addition, the expression of Cx43 and GJIC was closely related to the regulation of E2 and TGF-β1, and E2 treatment in turn restored the inhibition of TGF-β1 on GJIC. Conclusions: Our results indicate, for the first time in adult rat Leydig cells, that TGF-β1 suppresses P450arom activity, as well as the expression of the Cyp19 gene, and that depression of E2 secretion leads to down-regulation of Cx43-based GJIC between Leydig cells. 

Retracted: No

PubPeer comments:
 Figure 3A. * Green boxes: two panels representing different experiments look unexpectedly similar. ![file] ,
Generation of an induced pluripotent stem cell line (UNCCi002-A) from a healthy donor using a non-integration system to study Cerebral Cavernous Malformation (CCM)
Authors: Ariana Marquez
Sarahi G Molina
Adriana S Beltran
Alvaro A Beltran
Lorena J Munoz
Jose F Olivares
Journal: Stem Cell Research (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: induced pluripotent stem cells; healthy individuals; disease modeling; drug discovery; reprogramming
Affiliations: UNC Neuroscience Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States., Human Pluripotent Stem Cell Core, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States., Department of Pharmacology at the University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States., Human Pluripotent Stem Cell Core, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States; Department of Genetics at the University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States. Electronic address: .

Abstract:  The generation of induced pluripotent stem cells (iPSCs) from healthy individuals is an invaluable resource as reference control in disease modeling and drug discovery. This paper details the reprogramming of peripheral blood mononuclear cells (PBMCs) isolated from a healthy 27 years-old male using non-integration technology. The derived iPSCs displayed typical pluripotent stem cell morphology, the capacity to differentiate into the three germ layers, and normal karyotype. This iPSC line will be used as a reference control to study the Cerebral Cavernous Malformation disease mechanism. 

Retracted: No

PubPeer comments:
 The authors of this paper have registered this cell line as UNCi002-A in hPSCreg: https: hpscreg.eu cell-line UNCi002-A but have used an incorrect designatioin in their paper (UNCCi0002-A instead of UNCi002-A). Unfortunatly the lack of QC on the Stem Cell Researc  Lab Resources papers by Elsevier make this type of error more and more frequent. It seems Elsevier only care in maximizing their profit from this series of paper while not doing anything to insure that these papers abide to the rules that they have set themselves. Furthermore the URL in the  Cell line repository bank section does not resolve to a correct page and should be changed to: https: www.med.unc.edu humancellcore ( humancellcore instead of  humanstemcellcore ). Again Elsevier does not even check URLs provided in papers they publish. ,
Tumstatin induces apoptosis and stimulates phosphorylation of p65NF-κB in human osteoblastic osteosarcoma Saos-2 cells
Authors: Yang Wang
Jia-Song Teng
Ruo-Feng Yin
Journal: Oncology reports (2016)
Discipline: CLINICAL MEDICINE
Keywords: tumstatin; proliferation; apoptosis; Saos-2 cells; mechanism
Affiliations: Department of Orthopaedics, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China., Department of Orthopaedics, Daqing Oilfields general Hospital, Daqing, Heilongjiang 163000, P.R. China.

Abstract:  The present study was aimed to investigate the effect of tumstatin on inhibition of proliferation and induction of apoptosis in Saos-2 human osteosarcoma cells and to understand the mechanism involved. Inhibition of cell proliferation was analyzed by MTT assay and induction of apoptosis through nuclear fragmentation assay. Viability of Saos-2 cells was reduced to 19% on treatment with 25 µM concentration of tumstatin after 48 h. Presence of characteristic apoptotic nuclei, rounded cell shape and shrunken size were caused by tumstatin treatment at 25 µM concentration. The level of mRNA corresponding to PTEN, FasR and FasL was increased significantly in tumstatin treated Saos-2 cells compared to untreated control. Investigation of the mechanism revealed NF-κB activation by phosphorylation on serine 536. The activated NF-κB was translocated into the nucleus from the cytoplasm on treatment with tumstatin. Degradation of the IκBα by tumstatin was found to be much slower compared to that induced by treatment with TNF-α. Thus, tumstatin inhibits proliferation and induces apoptosis in Saos-2 cells through activation of NF-κB and its translocation to the nucleus. Therefore, tumstatin can play an important role in the treatment of osteosarcoma. 

Retracted: No

PubPeer comments:
  Figure 2 - Nuclear fragmentation of Saos-2 cells treated with tumstatin. (A) Nuclear morphology of Saos-2 cells treated with tumstatin. Saos-2 cells were treated for 48 h with tumstatin. Cells were stained with Hoechst 33342 and observed under a fluorescent microscope. Bar represents 10 u00b5m. (B) DNA ladder formation in tumstatin-treated Saos-2 cells. Saos-2 cells were exposed for 48 h to various concentrations of tumstatin indicated. DNA was extracted and analyzed on an agarose gel. Lane M, standard DNA markers; arrow indicates 500 bp. There is no scale bar. There is no Figure 2(B). Possibly this is for the best. Figure 2(A) is enough of an eyesore. Evidently the reviewers looked at this travesty and thought  Yes, that s just how cells like up on a microscope slide. Clone-stamping and sharp-edged rectangles are perfectly normal . ![file] , 
 Figs 4 and 5, together. ![file] I would go on, but [Figure 6] and [Figure 7] destroyed my will to live. ,
Comparison of PCR-RFLP and PFGE for determining the clonality of Brucella isolates from human and livestock specimens
Authors: Mohammad Yousef Alikhani
Mohammad Reza Arabestani
Nasrin Bahmani
Parviz Mohajerie
Seyed Hamid Hashemi
Reza Mirnejad
Manoochehr Karami
Journal: Saudi Journal of Biological Sciences (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Brucella melitensis; Brucellosis; Molecular typing; PCR; RFLP.
Affiliations: Brucellosis Research Center, Hamadan University of Medical Sciences, Hamadan, Iran., Molecular Biology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran., Department of Microbiology, Kermanshah University of Medical Sciences, Kermanshah, Iran., Department of Epidemiology, Hamadan University of Medical Sciences, Hamadan, Iran., Department of Microbiology, Hamadan University of Medical Sciences, Hamadan, Iran.

Abstract:  Brucellosis is an important zoonotic disease caused by different species of genus Brucella that are pathogenic for humans and a variety of animals. Accurate detection of Brucella spp. infection is important for control of disease. The aim of this study was to comparison of molecular genotyping of Brucella strains by Pulsed-field gel electrophoresis (PFGE) and polymerase chain reaction -Restriction Fragment Length Polymorphism (PCR-RFLP) techniques. Twenty- seven Brucella spp. were isolated from human and animal samples. The isolates identified by conventional microbiological methods and confirmed using PCR for amplification of omp2a gene. Molecular typing of Brucella strains carried out by PCR-RFLP after PstI and PFGE of chromosomal DNA after XbaI enzyme digestion. The omp2a gene PCR Products with different patterns of PCR-RFLP were sequenced. The omp2a gene amplification of all human and animal Brucella isolates were positive for 1100 bp fragment. By PCR-RFLP analysis two genotypes/patterns for human isolates and four genotypes for animal isolates were obtained. In PFGE analysis totally, 7 common clones/clusters and 3 single clones were obtained. The results of this study showed the PFGE method is the more reliable and useful assay for molecular typing of Brucella strains and is more preferred to PCR-RFLP in determination of genetic similarity among human and animal Brucella isolates. The presented data showed PCR-RFLP analysis was not able to differentiate between B. melitensis biovars and vaccine strain. 

Retracted: No

PubPeer comments:
 ![file] There are several undeclared splice sites in the immunoblots in Figure 3C. The bands in the blue boxes show unexpected similarity (WT HK group) in Figure 7C. Could authors provide an explanation, please? ,
Long noncoding RNA HAGLROS regulates apoptosis and autophagy in Parkinson’s disease via regulating miR-100/ATG10 axis and PI3K/Akt/mTOR pathway activation
Authors: Jingtao Wang
Xiaoyan Liu
Zhenqiang Fu
Hong Lu
Jingjing Lu
Guifang Sun
Xingrong Ma
Yu Liu
Tao Peng
Junmin Li
Wencui Wan
Yangfei Ji
Journal: Artificial Cells Nanomedicine and Biotechnology (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: ATG10 phosphoinositide-3 kinase/protein kinase-B/mammalian target of rapamycin pathway; HAGLROS; Parkinson’s disease; miR-100.
Affiliations: a Department of Neurology, Key-Disciplines Laboratory Clinical Medicine of Henan, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China., b Department of Ophthalmology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou , China.

Abstract:  Parkinson's disease (PD) is a common age-related neurodegenerative disease resulted from the progressive degeneration of dopaminergic neurons in the pars compacta region of substantia nigra. The goal of this study was to investigate the effects and mechanisms of long noncoding RNA (lncRNA) HAGLROS on the apoptosis and autophagy in PD. The MPTP-induced PD mouse model and MPP+-intoxicated SH-SY5Y cell model were established, and the expression levels of HAGLROS and miR-100 were determined. Subsequently, the effects of suppression of HAGLROS on apoptosis and autophagy in MPTP-induced PD mouse model and in MPP+-intoxicated SH-SY5Y cells were investigated. In addition, the association between HAGLROS and miR-100 as well as HAGLROS and activation of phosphoinositide-3 kinase/protein kinase-B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway in MPP+-intoxicated SH-SY5Y cells was explored. HAGLROS was increasingly expressed in MPTP-induced PD mouse model and MPP+-intoxicated SH-SY5Y cells and suppression of HAGLRO decreased apoptosis and autophagy in both in vivo and in vitro PD models. Further in vitro studies showed that HAGLRO negatively regulated miR-100 expression, and HAGLROS regulated apoptosis and autophagy of MPP+-intoxicated SH-SY5Y cells through sponging miR-100. Moreover, ATG10 was identified as a target of miR-100. Besides, suppression of HAGLROS alleviated MPP+-intoxicated SH-SY5Y cell injury by activating PI3K/AKT/mTOR pathway. Our findings reveal that upregulation of HAGLROS may contribute to the development of PD via inhibiting apoptosis and autophagy, which may be achieved by regulating miR-100/ATG10 axis and PI3K/AKT/mTOR pathway activation. 

Retracted: No

PubPeer comments:
 Figures 6C and 6D appear to show a repeated band. *** ![file] , 
 #1 Figure 5. ... (D) L-02 cells were pretreated with LY294002 (20 u03bcM) for 1 h, followed by treatment with SHK and LY294002 for 8 h, and then the Nrf2 protein levels were evaluated by Western blotting. ![file] ,
PDLIM4, an actin binding protein, suppresses prostate cancer cell growth
Authors: Charles Y F Young
Michael E Grossmann
John C Cheville
Katalin Ajtai
Thomas P Burghardt
Jin San Zhang
Donkena Krishna Vanaja
Aiyu Gong
Mozammel H Gazi
Journal: Cancer Investigation (2009)
Discipline: CLINICAL MEDICINE
Keywords: PDLIM4; prostate cancer cells; tumor suppressor; cell proliferation; actin
Affiliations: Department of Urology, Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN 55905, USA.

Abstract:  We investigated the molecular function of PDLIM4 in prostate cancer cells. PDLIM4 mRNA and protein-expression levels were reduced in LNCaP, LAPC4, DU145, CWR22, and PC3 prostate cancer cells. The re-expression of PDLIM4 in prostate cancer cells has significantly reduced the cell growth and clonogenicity with G1 phase of cell-cycle arrest. We have shown the direct interaction of PDLIM4 with F-actin. Restoration of PDLIM4 expression resulted in reduction of tumor growth in xenografts. These results suggest that PDLIM4 may function as a tumor suppressor, involved in the control of cell proliferation by associating with actin in prostate cancer cells. 

Retracted: No

PubPeer comments:
 Figure 1B. * Red boxes: Three lanes in the PDLIM4 panel (the protein of interest of this paper) appear to look more similar to each other than expected. ![file] ,
Asparagus racemosus competitively inhibits in vitro the acetylcholine and monoamine metabolizing enzymes
Authors: A V Muruganandam
Rakesh Ojha
Sairam Krishnamurthy
Jairam Meena
Journal: Neuroscience letters (2011)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Asparagus racemosus; antidepressant activity; cholinergic system; monoaminergic system; enzyme inhibitory activities
Affiliations: Neurotherapeutics Lab, Department of Pharmaceutics, Institute of Technology, Banaras Hindu University, Varanasi 221005, India.

Abstract:  Asparagus racemosus (AR) has earlier been reported to possess antidepressant activity possibly mediated through the monoaminergic system, and nootropic and anti amnestic activities possibly through the cholinergic system. In the present study to further understand the mechanism of action, we evaluated the kinetics of acetyl (AChE) and butyryl (BuChE) cholinesterases, and monoamine oxidase (MAO-A and B) enzyme inhibitory activities of different fractions of AR. The results showed that methanolic extract of AR (MAR) significantly inhibited cholinesterase and MAO activities as compared to hexane (HAR) and chloroform (CAR) extracts of AR as evident from the IC(50) values. The kinetic analysis of enzyme inhibition of MAR shows that the V(max) does not change with different concentrations of MAR but the K(m) value increases. This indicates that MAR is a non-selective competitive inhibitor for both cholinesterase and monoamine oxidase enzymes. Evaluation of K(i) values show that MAR inhibited these enzymes less potently compared to the respective standard drugs. There seems to be a positive correlation between the saponin content and, cholinesterase and monoamine inhibitory activities as MAR had 62.20% of saponins, whereas HAR and CAR had no measurable saponin content. The non-selective competitive inhibitory activity on cholinesterase and monoamine oxidase enzymes can explain many reported neuropharmacological activities of AR. AR apart being used as a drug is also used as a food. As such AR may have potential drug-drug, drug-food and food-food interactions with drugs and foods sharing the cholinergic and monoaminergic pathways. 

Retracted: No

PubPeer comments:
 I will admit that my knowledge of enzyme kinetics is very small. Still, it is rare in biology to do multiple measurements and find exactly the same values each time. Could the authors explain how in the VMax column in Table 2 all three inhibitors for ACS and two out of three inhibitors for BCS are reported with the exact same mean and Standard Deviation (or SEM, not sure)? Marked here with red and blue boxes. How many replicate experiments were performed in this table? Table 4 has similar concerns as well. ![file] ,
Effects of propofol on colon cancer metastasis through STAT3/HOTAIR axis by activating WIF-1 and suppressing Wnt pathway
Authors: Xi-Hua Lu
Yi Zhou
Chang-Sheng Li
Yun-Fei Zhang
Journal: Cancer medicine (2020)
Discipline: CLINICAL MEDICINE
Keywords: STAT3; Wnt signaling; colon cancer; lncRNA HOTAIR; propofol.
Affiliations: Department of Anesthesiology Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital Zhengzhou P.R. China

Abstract:  Background: In the present study, we aim to investigate the potential role of propofol in the tumor progression of colon cancer. Methods: Human colon cancer cell lines were cultured and exposed with 8 μg/mL propofol. RNA interference was performed to silence the expression of HOTAIR or STAT3 to explore their biological functions in colon cancer. Cell apoptosis and invasion were assessed using flow cytometry and transwell assays, respectively. Quantitative real-time PCR, western blot, and immunohistochemistry were subjected to measure the expression patterns of HOTAIR, STAT3, Wnt signaling factors, and epithelial-mesenchymal transition-related markers, respectively. Besides, nude mice were transplanted with colon cancer cells for further exploration. Tumor formation, volume, and weight were evaluated to validate the in vitro findings. Results: Propofol treatment promoted cell apoptosis and inhibited cell invasion in colon cancer cells, while the effects were reversed by HOTAIR overexpression. Additionally, STAT3 positively regulated HOTAIR expression, which was also negatively modulated by propofol. Moreover, STAT3 and HOTAIR were shown to independently regulate colon cancer cell apoptosis and invasion. Furthermore, HOTAIR could stimulate Wnt signaling pathway via inhibiting WIF-1 expression and upregulating β-catenin expression, which was also demonstrated by in vivo study. Conclusion: Taken together, the current study demonstrated that propofol exerts the inhibition on cell invasion and promotion on cell apoptosis through regulating STAT3/HOTAIR by activating WIF-1 and suppressing Wnt pathway, indicating that propofol might serve as a therapeutic role for colon cancer patients in the future. 

Retracted: No

PubPeer comments:
 In Figure 4A, three flow cytometry dot plots have been duplicated and presented as something else. The duplicated plots have been modified a bit (contrast brightness adjustments). ![file] ,
Effect of Ser-129 phosphorylation on interaction of α-synuclein with synaptic and cellular membranes
Authors: Anurag Tandon
Gang Zhang
Sabine Wislet-Gendebien
Isabelle Aubert
Naomi P Visanji
Paul E Fraser
Loren W Oschipok
Journal: Journal of Biological Chemistry (2011)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: α-synuclein; phosphorylation; Parkinson disease; Lewy bodies; Ser(P)-129
Affiliations: Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario M5S 3H2, Canada.

Abstract:  In the healthy brain, less than 5% of α-synuclein (α-syn) is phosphorylated at serine 129 (Ser(P)-129). However, within Parkinson disease (PD) Lewy bodies, 89% of α-syn is Ser(P)-129. The effects of Ser(P)-129 modification on α-syn distribution and solubility are poorly understood. As α-syn normally exists in both membrane-bound and cytosolic compartments, we examined the binding and dissociation of Ser(P)-129 α-syn and analyzed the effects of manipulating Ser(P)-129 levels on α-syn membrane interactions using synaptosomal membranes and neural precursor cells from α-syn-deficient mice or transgenic mice expressing human α-syn. We first evaluated the recovery of the Ser(P)-129 epitope following either α-syn membrane binding or dissociation. We demonstrate a rapid turnover of Ser(P)-129 during both binding to and dissociation from synaptic membranes. Although the membrane binding of WT α-syn was insensitive to modulation of Ser(P)-129 levels by multiple strategies (the use of phosphomimic S129D and nonphosphorylated S129A α-syn mutants; by enzymatic dephosphorylation of Ser(P)-129 or proteasome inhibitor-induced elevation in Ser(P)-129; or by inhibition or stable overexpression of PLK2), PD mutant Ser(P)-129 α-syn showed a preferential membrane association compared with WT Ser(P)-129 α-syn. Collectively, these data suggest that phosphorylation at Ser-129 is dynamic and that the subcellular distribution of α-syn bearing PD-linked mutations, A30P or A53T, is influenced by the phosphorylation state of Ser-129. 

Retracted: Yes

PubPeer comments:
 ![file] , 
 In light of this and other concerns about papers from one of the authors, it seems reasonable to point out a possible similarity between the WT and A30P pS129 panels in Figure 4B, highlighted here with red boxes. Could the authors please show the original, uncropped blots to take away any concerns? ![file] , 
 September 2020 withdrawal: https: www.jbc.org content 295 39 13695.short * This article has been withdrawn by Naomi Visanji, Sabine Wislet-Gendebien, Loren Oschipok, Isabelle Aubert, Paul Fraser, and Anurag Tandon. Gang Zhang was not reachable. The pS129 immunoblot in Fig. 1 was used for both membrane and cytosol fractions. In Fig. 4B, the pS129 blots from representative WT and A30P tissues are the same.* , 
 https: retractionwatch.com 2020 09 30 author-says-misguided-efforts-for-the-ideal-western-blot-led-to-the-withdrawal-of-these-studies ,
Transformation by v-Src: Ras-MAPK and PI3K-mTOR mediate parallel pathways
Authors: E Penuel
G S Martin
Journal: Molecular Biology of the Cell (1999)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Ras; transformation; v-Src; PI3K; mTOR
Affiliations: Department of Molecular and Cell Biology, University of California-Berkeley, Berkeley, California 94720-3204

Abstract:  An increase in the level of active, GTP-bound Ras is not necessary for transformation of chicken embryo fibroblasts (CEF) by v-Src. This suggests that other Ras-independent pathways contribute to transformation by v-Src. To address the possibility that activation of phosphatidylinositol-3-kinase (PI3K) and the mammalian target of rapamycin (mTOR/FRAP), represents one of these pathways, we have examined the effect of simultaneous inhibition of the Ras-MAPK and PI3K-mTOR pathways on transformation of CEF by v-Src. Transformation was assessed by the standard parameters of morphological alteration, increased hexose uptake, loss of density inhibition, and anchorage-independent growth. Inhibition of the Ras-MAPK pathway by expression of the dominant-negative Ras mutant HRasN17 or by addition of the MAPK kinase (MEK) inhibitor PD98059 reduced several of these parameters but failed to block transformation. Similarly, inhibition of the PI3K-mTOR pathway by addition of the PI3K inhibitor 2-[4-morpholinyl]-8-phenyl-4H-1-benzopyran-4-one (LY294002) or the mTOR inhibitor rapamycin, although reducing several parameters of transformation, also failed to block transformation. However, simultaneous inhibition of signaling by the Ras-MAPK pathway and the PI3K-mTOR pathway essentially blocked transformation. These data indicate that transformation of CEF by v-Src is mediated by two parallel pathways, the Ras-MAPK pathway and the PI-3K-mTOR pathway, which both contribute to transformation. The possibility that simultaneous activation of other pathways is also required is not excluded. 

Retracted: No

PubPeer comments:
 Figure 5 A and B should represent two different conditions (no treatment or cells treated with PD98059), but they seem to be same picture. ![file] ,
MicroRNA-192 suppresses liver metastasis of colon cancer
Authors: J Wang
J L Wisecarver
G Talmon
L Geng
A Chaudhuri
M Brattain
C Are
Journal: Oncogene (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Metastasis; colon cancer; microRNA; miR-192; apoptosis
Affiliations: Eppley Institute for Research in Cancer and Allied Diseases, Omaha, NE, USA., Department of Pathology and Microbiology, Omaha, NE, USA., Department of Surgical Oncology, Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE, USA., 1] Eppley Institute for Research in Cancer and Allied Diseases, Omaha, NE, USA [2] Department of Genetics, Cell Biology and Anatomy, Omaha, NE, USA [3] Department of Biochemistry and Molecular Biology, Omaha, NE, USA.

Abstract:  Metastasis causes most deaths from colon cancer yet mechanistic understanding and therapeutic options remain limited. Here we show that expression of microRNA (miR)-192 is inversely correlated with metastatic potential of colon cancer cells. Ectopic expression of miR-192 sensitizes colon cancer cells to growth factor deprivation stress-induced apoptosis, whereas inhibition of miR-192 confers resistance. Overexpression of miR-192 inhibits metastatic colonization to the liver in an orthotopic mouse model of colon cancer. Alterations associated with the metastatic phenotype in the primary tumors include increased apoptosis, decreased proliferation and angiogenesis. Further studies indicate that miR-192 downregulates expression of Bcl-2, Zeb2 and VEGFA in vitro and in vivo, which is responsible for enhanced apoptosis, increased expression of E-cadherin and decreased angiogenesis in vivo, respectively. Finally, studies performed on human colonic adenocarcinoma show that expression of miR-192 is significantly reduced in neoplastic cells as compared with normal colonic epithelium. Importantly, there is a significant decrease in miR-192 expression in stage IV tumors when compared with stage I or II lesions. These findings indicate that miR-192 has an important role in colon cancer development and progression. Our studies underscore the clinical relevance and prognostic significance of miR-192 expression in colon cancer. Therefore, a major implication of our studies is that restoration of miR-192 expression or antagonism of its target genes (Bcl-2, Zeb2 or VEGFA) may have considerable therapeutic potential for anti-metastatic therapy in patients with colon cancer. 

Retracted: No

PubPeer comments:
 Per last author, this paper has a pending correction. Discussed here: https: pubpeer.com publications AC6BA6D6B0CA0C999DD2CEE3BA4B25 *** ![file] , 
 Dear Actinopolyspora, We have mistakenly used a wrong actin image when preparing the figure. Please see the uploaded original data and corrected Fig. 2A. We apologize for the mistake and thank you for helping us correct it. Best, Jing Wang ![file] ,