PReD-Bench/PRed-Bench huggingface dataset:
Glutathione depletion induced by c-Myc downregulation triggers apoptosis on treatment with alkylating agents
Authors: Barbara Benassi
Gabriella Zupi
Francesco Fiorentino
Annamaria Biroccio
Journal: Neoplasia (0)
Discipline: CLINICAL MEDICINE
Keywords: c-Myc; drug response; melanoma cells; alkylating agents; cisplatin
Affiliations: Experimental Chemotherapy Laboratory, Experimental Research Center, Regina Elena Cancer Institute, Rome 00158, Italy. 

Abstract:  Here we investigate the mechanism(s) involved in the c-Myc-dependent drug response of melanoma cells. By using three M14-derived c-Myc low-expressing clones, we demonstrate that alkylating agents, cisplatin and melphalan, trigger apoptosis in the c-Myc antisense transfectants, but not in the parental line. On the contrary, topoisomerase inhibitors, adriamycin and camptothecin, induce apoptosis to the same extent regardless of c-Myc expression. Because we previously demonstrated that c-Myc downregulation decreases glutathione (GSH) content, we evaluated the role of GSH in the apoptosis induced by the different drugs. In control cells treated with one of the alkylating agents or the others, GSH depletion achieved by L-buthionine-sulfoximine preincubation opens the apoptotic pathway. The apoptosis proceeded through early Bax relocalization, cytochrome c release, and concomitant caspase-9 activation, whereas reactive oxygen species production and alteration of mitochondria membrane potential were late events. That GSH was determining in the c-Myc-dependent drug-induced apoptosis was demonstrated by altering the intracellular GSH content of the c-Myc low-expressing cells up to the level of controls. Indeed, GSH ethyl ester-mediated increase of GSH abrogated apoptosis induced by cisplatin and melphalan by inhibition of Bax/cytochrome c redistribution. The relationship among c-Myc, GSH content, and the response to alkylating agent has been also evaluated in the M14 Myc overexpressing clones as well as in the melanoma JR8 c-Myc antisense transfectants. All together, these results demonstrate that GSH plays a key role in governing c-Myc-dependent drug-induced apoptosis. 

Retracted: No

PubPeer comments:
null, 
 ![file] , 
null, 
 Figure 6a. Vertical, sharp edges. ![file] , 
 #3 There is probably another one. ![file] Here compared after a slight adjustment: ![file] ,
Cleavage of the Junin virus nucleoprotein serves a decoy function to inhibit the induction of apoptosis during infection
Authors: Svenja Wolff
Stephan Becker
Allison Groseth
Journal: Journal of Virology (2013)
Discipline: MICROBIOLOGY
Keywords: apoptosis regulation; arenavirus infection; Junin virus; nucleoprotein cleavage; caspase cleavage motifs
Affiliations: Institut für Virologie, Philipps Universität Marburg, Marburg, Germany.

Abstract:  The regulation of apoptosis during infection is an important factor for host survival and, in some cases, also for the virus life cycle. At the same time, mechanisms to prevent the induction of apoptosis have been observed in numerous viral pathogens, but until now the role of apoptosis during arenavirus infection has not been investigated. Junin virus (JUNV) belongs to the New World arenavirus serogroup of the Arenaviridae and is the causative agent of Argentine hemorrhagic fever. We have demonstrated that infection with JUNV in cell culture does not induce apoptosis but leads to cleavage of the nucleoprotein (NP) into discrete products resembling caspase cleavage events. Similar specific NP degradation patterns were also observed in NP-transfected cell lines, and a closer examination of the sequence of NP showed several putative caspase cleavage motifs. Point mutations that abolished these cleavage motifs were consistent with the loss of certain cleavage products. Consistent with these data, further studies showed that treatment with a caspase inhibitor also reduced NP cleavage, indicating that the observed cleavage events were occurring as a result of caspase activity with NP as a substrate. Finally, we showed that expression of NP suppresses the cleavage of caspase 3 in cells treated with an apoptosis activator. Based on these findings, we propose that NP functions as a decoy substrate for caspase cleavage in order to inhibit the induction of apoptosis in JUNV-infected cells. 

Retracted: No

PubPeer comments:
 Figure 1 shows unexpected similarity of noise in XRD patterns of Fe3O4@MWCNT and MWCNT. ![file] , 
 ![file] , 
 ![file] Number of layers is different. Is it really the same region? , 
 This paper is one of 30+ (38 and counting) papers by the same research group that all share the same photo. In all papers, this photo is used as a zoomed-in inset representing the high-resolution transmission electron microscopy (HRTEM) analysis of the  atomic lattice fringe and particle size of the nanoparticles. Of concern, the same photo is used to represent a different type of nanoparticle in each of these papers. Here is a collage of 6 different uses of the same photo,  Inset 1 : ![file] A list of the first 30 papers that all use this photo, and the different types of nanoparticles that they represent can e.g. be found here: * Betuu0308l Su0327en et al. - DOI: 10.1016 j.ijhydene.2018.03.175 - https: pubpeer.com publications 8AD71F4A32472314CCE9983D47E36F Here is Figure 2 of this paper that includes the  Inset1 photo: ![file] ,
MicroRNA-34A inhibits the growth, invasion and metastasis of gastric cancer by targeting PDGFR and MET expression
Authors: Jin-Jun Guo
Yan-Min Liu
Xiao-Ling Wu
Yang Peng
Journal: Bioscience Reports (2014)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: RTKs; PDGFR; miRNAs; mRNAs; cancer
Affiliations: *Department of Gastroenterology and Hepatology, The Second Affiliated Hospital of Chongqing Medical University, 74 Linjiang Road, Chongqing 400010, China.

Abstract:  Within the family of RTKs (receptor tyrosine kinases), PDGFR (platelet-derived growth factor receptor) has been implicated in carcinogenesis and tumour development. miRNAs (microRNAs), which can target the mRNAs (messenger RNAs) of cancer-associated genes, are abnormally expressed in various cancers. In this study, our aim was to identify the miRNAs that target PDGFR-α/β and to study the functions of these miRNAs. miR-34a was predicted to target PDGFR, and luciferase reporter assays showed that miR-34a could directly target PDGFR. Meanwhile, we found that miR-34a was down-regulated in gastric cancer tissues and was associated with metastasis. Our findings showed that miR-34a could inhibit gastric cancer cell migration, invasion and proliferation, but these tumourigenic properties were only partially restored when PDGFR-α/β was overexpressed. In subsequent experiments, we found that the overexpression of both PDGFR and MET could completely restore the gastric cancer tumourigenic properties. Moreover, the cancer-associated cell signalling pathway was studied, and we found that miR-34a could inhibit Akt [PKB (protein kinase B)] phosphorylation, which was restored by the overexpression of both PDGFR and MET. In conclusion, miR-34a may act as a potential tumour suppressor in gastric cancer and is associated with the mechanisms of gastric cancer metastasis; miR-34a can inhibit gastric cancer tumourigenesis by targeting PDGFR and MET through the PI3K (phosphoinositide 3-kinase)/Akt pathway. 

Retracted: No

PubPeer comments:
 Cyan boxes highlight apparent image overlap between this paper and the 2015 paper discussed here: https: pubpeer.com publications BC0D7198BC0B38B76625C6B4EC02C2 *** ![file] , 
 Figure 5c appears to have some image overlaps. *** ![file] *** Full figure ![file] , 
 (Posted in error) , 
 EXPRESSION OF CONCERN| APRIL 06 2021 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. ,
Arctiin abrogates osteoclastogenesis and bone resorption via suppressing RANKL-induced ROS and NFATc1 activation
Authors: Delong Chen
Meng Zhang
Ziyi Wang
Yun Liu
Zhen Ye
Qingqing Wang
Heng Qiu
Gangyu Zhang
Jinbo Yuan
Haibin Wang
Peng Chen
Gang Wang
Jacob Kenny
Junjian Wang
Jianbo He
Chao Wang
Fan Yang
Jiake Xu
Vincent Kuek
Journal: Pharmacological Research (2020)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Arctiin; Bone resorption; Osteoclast; RANKL-induced NFATc1 activation; ROS.
Affiliations: Guangzhou University of Chinese Medicine, Guangzhou 510405, China.

Abstract:  Osteoporosis, characterized by disrupted bone resorption and formation, is viewed as a global health challenge. Arctiin (ARC) is a main component of Arctium lappa L, which exerts chemopreventive effects against various tumor cells. However, the role of ARC in bone remodeling is still unclear. Here, we first demonstrated that ARC inhibits osteoclast formation and bone resorption function induced by the receptor activator of nuclear factor-κB ligand (RANKL) in a dose- and time-dependent manner without exerting cytotoxic effects. Mechanistic analysis revealed that ARC not only suppresses RANKL-induced mitogen-activated protein kinase (MAPK) and calcium signaling pathways, but also enhances the expression of cytoprotective enzymes that are involved in scavenging reactive oxygen species (ROS). Further, ARC inhibits the activation of the major transcription factor nuclear factor of activated T cells 1 (NFATc1) during RANKL-induced osteoclast formation. Preclinical studies showed that ARC protects bone loss in an ovariectomy (OVX) mouse model. Conclusively, our data confirmed that ARC could potentially inhibit osteoclastogenesis by abrogating RANKL-induced MAPK, calcium, and NFATc1 signaling pathway, as well as by promoting the expression of ROS scavenging enzymes in Nrf2/Keap1/ARE signaling pathway, thereby2 preventing OVX-induced bone loss. Thus, ARC may serve as a novel therapeutic agent for the treatment of osteoporosis. 

Retracted: No

PubPeer comments:
 Image duplication in Fig 3A ![file] ,
Superior X-ray Radiation Shielding Effectiveness of Biocompatible Polyaniline Reinforced with Hybrid Graphene Oxide-Iron Tungsten Nitride Flakes
Authors: Seyyed Mojtaba Mousavi
Seeram Ramakrishna
Seyyed Alireza Hashemi
Reza Faghihi
Chin Wei Lai
Sonia Bahrani
Mohammad Arjmand
Mansour Rahsepar
Journal: Polymers (2020)
Discipline: CHEMISTRY
Keywords: X-ray attenuation; anti-bacterial/anti-fungal; biocompatible; graphene oxide; polyaniline.
Affiliations: Department of Mechanical Engineering, Center for Nanofibers and Nanotechnology, National University of Singapore, Singapore 119077, Singapore., Department of Medical Nanotechnology, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz 71348-14336, Iran., Department of Chemical Engineering, National Taiwan University of Science and Technology, Taipei 10607, Taiwan., Nuclear Engineering Department, Shiraz University, Shiraz 71936-16548, Iran., Radiation Research Center, Shiraz University, Shiraz 71936-16548, Iran., School of Engineering, University of British Columbia, Kelowna, BC, V1V 1V7, Canada., Department of Materials Science and Engineering, School of Engineering, Shiraz University, Zand Boulevard, Shiraz 71348-51154, Iran., Nanotechnology & Catalysis Research Center, University of Malaya, Kuala Lumpur 50603, Malaysia.

Abstract:  X-ray radiation is a harmful carcinogenic electromagnetic source that can adversely affect the health of living species and deteriorate the DNA of cells, thus it's vital to protect vulnerable sources from them. To address this flaw, the conductive polymeric structure of polyaniline (PANi) was reinforced with diverse filler loadings (i.e., 25 wt % and 50 wt %) of hybrid graphene oxide-iron tungsten nitride (ITN) flakes toward attenuation of X-ray beams and inhabitation of microorganisms' growth. Primary characterizations confirmed the successful decoration of graphene oxide (GO) with interconnected and highly dense structure of iron tungsten nitride with a density of about 24.21 g.cm⁻3 and reinforcement of PANi with GO-ITN. Additionally, the outcome of evaluations showed the superior performance of developed shields, where a shield with 1.2 mm thickness containing 50 wt % GO-ITN showed 131.73 % increase in the electrical conductivity (compared with neat PANi) along with 78.07%, 57.12%, and 44.99% decrease in the amplitude of the total irradiated X-ray waves at 30, 40, and 60 kVp tube voltages, respectively, compared with control X-ray dosage. More importantly, the developed shields not only showed non-toxic nature and improved the viability of cells, but also completely removed the selected microorganisms at a concentration of 1000 µg.mL-1. 

Retracted: No

PubPeer comments:
 Authors forgotten to show original spectra. Not even envelope of the peaks is provided. ![file] ,
Involvement of dihydroceramide desaturase in cell cycle progression in human neuroblastoma cells
Authors: Zdzislaw M Szulc
Yusuf A Hannun
Alicja Bielawska
Jacek Bielawski
Besim Ogretmen
Lina M Obeid
Jacqueline M Kraveka
Li Li
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: dihydroceramide desaturase; ceramide generation; neuroblastoma cells; desaturase activity; liquid chromatography/mass spectrometry
Affiliations: Division of Hematology/Oncology, Department of Pediatrics, Medical University of South Carolina, Charleston, South Carolina 29425, USA. 

Abstract:  The role of dihydroceramide desaturase as a key enzyme in the de novo pathway of ceramide generation was investigated in human neuroblastoma cells (SMS-KCNR). A novel assay using water-soluble analogs of dihydroceramide, dihydroceramidoids (D-erythro-dhCCPS analogs), was used to measure desaturase activity in situ. Conversion of D-erythro-2-N-[12'-(1''-pyridinium)-dodecanoyl]-4,5-dihydrosphingosine bromide (C(12)-dhCCPS) to its 4,5-desaturated counterpart, D-erythro-2-N-[12'-(1''-pyridinium)dodecanoyl]sphingosine bromide (C(12)-CCPS), was determined by liquid chromatography/mass spectrometry analysis. The validity of the assay was confirmed using C(8)-cyclopropenylceramide, a competitive inhibitor of dihydroceramide desaturase. A human homolog (DEGS-1) of the Drosophila melanogaster des-1 gene was recently identified and reported to have desaturase activity. Transfection of SMS-KCNR cells with small interfering RNA to DEGS-1 significantly blocked the conversion of C(12)-dhCCPS to C(12)-CCPS. The associated accumulation of endogenous dihydroceramides confirmed DEGS-1 as the main active dihydroceramide desaturase in these cells. The partial loss of DEGS-1 inhibited cell growth, with cell cycle arrest at G(0)/G(1). This was accompanied by a significant decrease in the amount of phosphorylated retinoblastoma protein. This hypophosphorylation was inhibited by tautomycin and not by okadaic acid, suggesting the involvement of protein phosphatase 1. Additionally, we found that treatment of SMS-KCNR cells with fenretinide inhibited desaturase activity in a dose-dependent manner. An increase in dihydroceramides (but not ceramides) paralleled this process as measured by liquid chromatography/mass spectrometry. There were no effects on the mRNA or protein levels of DEGS-1, suggesting that fenretinide acts at the post-translational level as an inhibitor of this enzyme. Tautomycin was also able to block the hypophosphorylation of the retinoblastoma protein observed upon fenretinide treatment. These findings suggest a novel biological function for dihydroceramides. 

Retracted: No

PubPeer comments:
 The immunoblot for actin and Rb in red box appear to look similar in Fig. 5C. ![file] , 
 The immunoblot for actin in Fig. 5C appears similar to that in Fig. 7B, although the experimental conditions were different, and the pRb immunoblots are different. ![file] ,
Human Mitochondrial Leucyl-tRNA Synthetase Corrects Mitochondrial Dysfunctions Due to the tRNA Leu(UUR) A3243G Mutation, Associated with Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-Like Symptoms and Diabetes
Authors: Ronghua Li
Min-Xin Guan
Journal: Molecular and cellular biology (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Mitochondrial tRNA genes; A3243G mutation; mitochondrial encephalomyopathy; lactic acidosis; stroke-like symptoms
Affiliations: Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio

Abstract:  Mutations in mitochondrial tRNA genes are associated with a wide spectrum of human diseases. In particular, the tRNA(Leu(UUR)) A3243G mutation causes mitochondrial encephalomyopathy, lactic acidosis, and stroke-like symptoms (MELAS) and 2% of cases of type 2 diabetes. The primary defect in this mutation was an inefficient aminoacylation of the tRNA(Leu(UUR)). In the present study, we have investigated the molecular mechanism of the A3243G mutation and whether the overexpression of human mitochondrial leucyl-tRNA synthetase (LARS2) in the cytoplasmic hybrid (cybrid) cells carrying the A3243G mutation corrects the mitochondrial dysfunctions. Human LARS2 localizes exclusively to mitochondria, and LARS2 is expressed ubiquitously but most abundantly in tissues with high metabolic rates. We showed that the alteration of aminoacylation tRNA(Leu(UUR)) caused by the A3243G mutation led to mitochondrial translational defects and thereby reduced the aminoacylated efficiencies of tRNA(Leu(UUR)) as well as tRNA(Ala) and tRNA(Met). We demonstrated that the transfer of human mitochondrial leucyl-tRNA synthetase into the cybrid cells carrying the A3243G mutation improved the efficiency of aminoacylation and stability of mitochondrial tRNAs and then increased the rates of mitochondrial translation and respiration, consequently correcting the mitochondrial dysfunction. These findings provide new insights into the molecular mechanism of maternally inherited diseases and a step toward therapeutic interventions for these disorders. 

Retracted: No

PubPeer comments:
 August 2017 Correction found here: https: mcb.asm.org content 37 18 e00335-17 The Correction reads:  Fig. 4A: The sixth-row image was a duplicate of the fifth-row image. The corrected sixth-row image should appear as shown below. The conclusions remain unchanged by this correction. We apologize for any confusion this error might have caused. Here is the original Figure 4A, as reported to the paper in September 2016, with the duplication marked with green boxes. ![file] I thank the authors for correcting this error. This paper was part of a structured search for image duplications in Molecular and Cellular Biology paper, which was published here: https: mcb.asm.org content 38 20 e00309-18.long ,
A caveolin-3 mutant that causes limb girdle muscular dystrophy type 1C disrupts Src localization and activity and induces apoptosis in skeletal myotubes
Authors: Marie-Helene Disatnik
Joshua C Eby
Thomas A Rando
Gayle M Smythe
Journal: Journal of Cell Science (2003)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Caveolins; Caveolae; Src tyrosine kinases; Muscle-specific caveolin; Caveolin-3
Affiliations: Department of Neurology and Neurological Science, Stanford University School of Medicine, Stanford, California, 94305-5235, USA, Neurology Service and GRECC, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, 94304, USA

Abstract:  Caveolins are membrane proteins that are the major coat proteins of caveolae, specialized lipid rafts in the plasma membrane that serve as scaffolding sites for many signaling complexes. Among the many signaling molecules associated with caveolins are the Src tyrosine kinases, whose activation regulates numerous cellular functions including the balance between cell survival and cell death. Several mutations in the muscle-specific caveolin, caveolin-3, lead to a form of autosomal dominant muscular dystrophy referred to as limb girdle muscular dystrophy type 1C (LGMD-1C). One of these mutations (here termed the 'TFT mutation') results in a deletion of a tripeptide (DeltaTFT(63-65)) that affects the scaffolding and oligomerization domains of caveolin-3. This mutation causes a 90-95% loss of caveolin-3 protein levels and reduced formation of caveolae in skeletal muscle fibers. However, the effects of this mutation on the specific biochemical processes and cellular functions associated with caveolae have not been elucidated. We demonstrate that the TFT caveolin-3 mutation in post-mitotic skeletal myotubes causes severely reduced localization of caveolin-3 to the plasma membrane and to lipid rafts, and significantly inhibits caveolar function. The TFT mutation reduced the binding of Src to caveolin-3, diminished targeting of Src to lipid rafts, and caused abnormal perinuclear accumulation of Src. Along with these alterations of Src localization and targeting, there was elevated Src activation in myotubes expressing the TFT mutation and an increased incidence of apoptosis in those cells compared with control myotubes. The results of this study demonstrate that caveolin-3 mutations associated with LGMD-1C disrupt normal cellular signal transduction pathways associated with caveolae and cause apoptosis in muscle cells, all of which may reflect pathogenetic pathways that lead to muscle degeneration in these disorders. 

Retracted: No

PubPeer comments:
 ![file] , 
 Figure 3B. Splices in Cav-1 panel, but not in the Cav-3 or Actin panels. Also, 2nd lane Cav-1 panel is much wider than the other lanes. ![file] ,
Vimentin intermediate filament assembly regulates fibroblast invasion in fibrogenic lung injury
Authors: Ranu Surolia
Kevin Dsouza
Veena B Antony
Vinoy Thomas
Zheng Wang
Victor J Thannickal
Sergey Mirov
Mohammad Athar
Fu Jun Li
Dolores Pérez-Sala
Huashi Li
Journal: JCI Insight (2019)
Discipline: CLINICAL MEDICINE
Keywords: Autophagy; Drug therapy; Fibrosis; Pulmonology.
Affiliations: Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine., Department of Materials Science and Engineering, and., Department of Physics, University of Alabama at Birmingham (UAB), Birmingham, Alabama, USA., Department of Structural and Chemical and Biology, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas (CSIC), Madrid, Spain., Department of Dermatology, UAB, Birmingham, Alabama, USA.

Abstract:  Idiopathic pulmonary fibrosis (IPF) is a progressive disease, with a median survival of 3-5 years following diagnosis. Lung remodeling by invasive fibroblasts is a hallmark of IPF. In this study, we demonstrate that inhibition of vimentin intermediate filaments (VimIFs) decreases the invasiveness of IPF fibroblasts and confers protection against fibrosis in a murine model of experimental lung injury. Increased expression and organization of VimIFs contribute to the invasive property of IPF fibroblasts in connection with deficient cellular autophagy. Blocking VimIF assembly by pharmacologic and genetic means also increases autophagic clearance of collagen type I. Furthermore, inhibition of expression of collagen type I by siRNA decreased invasiveness of fibroblasts. In a bleomycin injury model, enhancing autophagy in fibroblasts by an inhibitor of VimIF assembly, withaferin A (WFA), protected from fibrotic lung injury. Additionally, in 3D lung organoids, or pulmospheres, from patients with IPF, WFA reduced the invasiveness of lung fibroblasts in the majority of subjects tested. These studies provide insights into the functional role of vimentin, which regulates autophagy and restricts the invasiveness of lung fibroblasts. 

Retracted: No

PubPeer comments:
 Fig 2 -- could the authors please check why control and starvation look so similar? ![file] ,
A community study of male androgenetic alopecia in Bishan, Singapore
Authors: H P Chia
L L Cheong
D Koh
P H Tang
Journal: Singapore Medical Journal (2000)
Discipline: CLINICAL MEDICINE
Keywords: Androgenetic alopecia; prevalence; male population; Norwood Criteria; survey
Affiliations: National University of Singapore, Singapore.

Abstract:  Background: Androgenetic alopecia is the most common form of hair loss. It affects a large number of the local male population, with 1,812 men seeking treatment for hair loss at the sole dermatological tertiary referral centre in Singapore in 1994. The aim of this study was to assess the prevalence of male androgenetic alopecia in the community. Methods: A questionnaire-based cross-sectional survey with a one-stage sampling method was conducted. Each male was diagnosed clinically and the severity graded according to the Norwood Criteria. The survey area was in Bishan East, a housing estate with 8,004 households. A total of 335 households were selected for the survey. Results: The household response rate was 84%. Within these households, 254 out of 378 men participated in the study (67% response rate). The prevalence of androgenetic alopecia was found to be 63%. The prevalence of the condition increased with age, from 32% among young adults aged 17 to 26 years to 100% among those in their 80s. Proportionately more Indians (87%) were affected compared to Chinese (61%). 81% of the respondents with androgenetic alopecia did not seek help as they did not view it as a problem. Of those seeking treatment, 74% used non-medical methods of unproven effectiveness. Conclusion: There is a high prevalence of androgenetic alopecia in the community in Singapore. Age specific prevalence and racial differences correlate well with both Western and local studies respectively. 

Retracted: No

PubPeer comments:
 This study has a potential conflict of interest which may have significantly skewed its results and framing (Perlis et al., 2005; Cosgrove et al., 2013). Specifically, at least one author (or author s employer) sold hair loss androgenetic alopecia products or services at the time of the research. Therefore, they may have financially profited when anyone saw the study and interpreted androgenetic alopecia hair loss to be distressing and in need of the products services sold by the author (or authoru2019s employer). Multiple authors work at a dermatology clinic offering hair loss interventions (National Skin Centre, no date.). The authors declare no conflicts in the journal. Sources Cosgrove, L, H J Bursztajn, D R Erlich, E E Wheeler, and A F Shaughnessy. u2018Conflicts of Interest and the Quality of Recommendations in Clinical Guidelinesu2019. Journal of Evaluation in Clinical Practice 19, no. 4 National Skin Centre. (no date). Dermatologists. Nsc.Com. URL: https: www.nsc.com.sg patient-guide our-doctors pages dermatologists.aspx Perlis, Clifford S., Michael Harwood, and Roy H. Perlis. u2018Extent and Impact of Industry Sponsorship Conflicts of Interest in Dermatology Researchu2019. Journal of the American Academy of Dermatology 52, no. 6 (1 June 2005): 967u201371. https: doi.org 10.1016 j.jaad.2005.01.020. ,
Cobalt metal–organic framework-based ZIF-67 for the trace determination of herbicide molinate by ion mobility spectrometry: investigation of different morphologies
Authors: Mohammad T Jafari
Ahmed Esmail Shalan
Fatemeh Davar
Mehdi Davoodi
Mohammad R Rezayat
Journal: RSC Advances (2021)
Discipline: CHEMISTRY
Keywords: Co-MOF; ZIF-67; morphologies; reaction conditions; cobalt source
Affiliations: Department of Chemistry, BCMaterials

Abstract:  Co-MOF-based zeolitic imidazolate frameworks (ZIF-67) with various morphologies were prepared via an innovative way under distinct reaction conditions. By changing the reaction conditions, including the cobalt source, solvent, time, temperature, and linking agent to the cobalt ions, the morphological evolution of Co-MOF-based ZIF-67 was investigated. The Co-MOF-based ZIF-67 was applied as an adsorbent fiber in the solid-phase microextraction (SPME) technique for extracting a herbicide, namely molinate (as a test compound), in aqueous samples. For recognizing the molinate molecules, drift tube ion mobility spectrometry (IMS) was employed as a sensitive, rapid, and simple detection technique. Two essential parameters, namely extraction temperature and extraction time, influenced the extraction efficiency, and these parameters were also analyzed and optimized. The linear dynamic range (LDR) and the determination coefficient were found to be 0.5-20.0 μg L-1 and 0.9990, respectively. In this regard, the limit of quantification (LOQ) and the detection limit (LOD) were calculated and found to be 0.5 μg L-1 and 0.15 μg L-1, respectively. Finally, the effect of the adsorbent with different morphologies on the extraction efficiency was compared. 

Retracted: No

PubPeer comments:
 Figures 6 and 7. In all rows, the d sample appears to look similar (shown with blue boxes). It might be the  isotypic control but the description is unclear, because the panels are labeled a-d, but the legends describe a, c, d, and e. ![file] Figure 6 legend:  Flow cytometric analyses of CD80 (A) and CD86 (B) markers on surface of APCs in the Balb c mice immunized with the vaccine formulations. Lymphocytes isolated from mice immunized with PB-PLGA-Cp (a), PLGA-Cp (c), PB-Cp (d), and isotypic control (e) in the panel (A) and similarly on the (B) were subjected to flow cytometric analysis as described under Section 2.  Figure 7 legend:  Fig. 7. Up-regulation of T lymphocytes in mice immunized with various vaccine formulations of Cp. Surface marker CD4 (A) and CD8 (B) present on the T cells population of animal immunized with PB-PLGA-Cp (a), PLGA-Cp (c), PB-Cp (d) and isotypic control (e) in the panel (A) and similarly in the panel (B) were subjected to flow cytometric analysis. In the bar graphs, the control samples are also shown to depict CD4+ or CD8+, not an isotype control. Shown here is Figure 7C: ![file] Could the authors clarify if all four panels d should look identical? ,
Hispidulin inhibits proliferation and enhances chemosensitivity of gallbladder cancer cells by targeting HIF-1α
Authors: Jianjun Peng
Jing Xie
Hui Gao
Chunbo Wang
Mei Han
Qixiao Jiang
Yantao Han
Journal: Experimental cell research (2015)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Chemosensitivity; Gallbladder cancer; HIF-1α; Hispidulin; P-gp.
Affiliations: Medical College, Qingdao University, Qingdao, Shandong 266071, China., College of Life Sciences, Chongqing Normal University, Chongqing 401331, China. Electronic address: ., Medical College, Qingdao University, Qingdao, Shandong 266071, China. Electronic address: .

Abstract:  Gallbladder cancer (GBC) is an aggressive malignancy of the bile duct, which is associated with a low (5-year) survival and poor prognosis. The transcription factor HIF-1α is implicated in the angiogenesis, cell survival, epithelial mesenchymal transition (EMT) and invasiveness of GBC. In this study, we have investigated the role of HIF-1α in the pathobilogy of GBC and effect of hispidulin on the molecular events controlled by this transcription factor. We observed that hispidulin caused induction of apoptosis, blockade of growth and cell cycle progression in GBC cells. Our results have demonstrated for the first time that hispidulin-exerted anti-tumor effect involved the suppression of HIF-1α signaling. Hispidulin was found to repress the expression of HIF-1α protein dose-dependently without affecting the HIF-1α mRNA expression. In addition, the inhibition of HIF-1α protein synthesis was revealed to be mediated through the activation of AMPK signaling. Hispidulin also sensitized the tumor cells to Gemcitabine and 5-Fluoroucil by down-regulating HIF-1α/P-gp signaling. Given the low cost and exceedingly safe profile, hispidulin appears to be a promising and novel chemosensitizer for GBC treatment. 

Retracted: No

PubPeer comments:
 This paper is one of a small collection of papers which appears to include a typographical error in the spelling of an manufacturer. The company name is ACEA Biosciences headquartered in San Diego. In this paper and the others, the name is spelled ACEC. This suggests that the paper was written from a common template, although the author groups are mostly different. Note: Of the papers with this apparent typo, this is the first Iu2019ve come across that does not appear to include authors affiliated with institutions in China. *** ![file] ,
Synergy between LRH-1 and beta-catenin induces G1 cyclin-mediated cell proliferation
Authors: Thomas Brennan
Céline Haby
Elisabeth Fayard
Kristina Schoonjans
Winston Thomas
Tatsuhiko Kodama
Olivia Wendling
Oronza A Botrugno
Toshiya Tanaka
Johan Auwerx
Jean-Sébastien Annicotte
Journal: Molecular Cell (2004)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LRH-1; orphan nuclear receptor; cell proliferation; cyclin D1; cyclin E1
Affiliations: Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique, Institut National de la Santé et de la Recherche Médicale, Université Louis Pasteur, 67404 Illkirch, France.

Abstract:  LRH-1 is an orphan nuclear receptor predominantly expressed in tissues of endodermal origin, where it controls development and cholesterol homeostasis. We show here that LRH-1 induces cell proliferation through the concomitant induction of cyclin D1 and E1, an effect that is potentiated by its interaction with beta-catenin. Whereas beta-catenin coactivates LRH-1 on the cyclin E1 promoter, LRH-1 acts as a potent tissue-restricted coactivator of beta-catenin on the cyclin D1 promoter. The implication of LRH-1 in cell proliferation highlights an unanticipated crosstalk between LRH-1 and the beta-catenin/Tcf4 signaling pathway, which is relevant for the renewal of intestinal crypt cells. 

Retracted: No

PubPeer comments:
 Figure 2C u2013 more similar than expected ![file] ,
MicroRNA-322 attenuates aluminum maltolate-induced apoptosis in the human SH-SY5Y neuroblastoma cell line
Authors: Yongzhi Shan
Jianxin Du
Qiuxia Zhang
Qingtang Lin
Feng Ling
Xinlong Ma
Shuo Han
Geng Xu
Hongqi Zhang
Feng Shang
Journal: Molecular Medicine Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: Aluminum-maltolate; apoptosis; microRNA-322; Alzheimer's disease; neuroblastoma
Affiliations: Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, P.R. China., School of Traditional Chinese Medicine, Capital Medical University, Beijing 100069, P.R. China., Human Anatomy Division, Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China.

Abstract:  Aluminum-maltolate (Al‑Malt) is a potent apoptosis inductor, which has been widely reported as an etiologic factor in Alzheimer's disease (AD). MicroRNA-322 (miR‑322) is a vital regulator in various biological processes. The aim of the current study was to identify the role and possible underlying mechanism of miR‑322 in Al‑Malt‑induced apoptosis. Eight concentrations of Al‑Malt were prepared and used for treating the human neuroblastoma cell line, SH‑SY5Y. Subsequent to treatment with Al‑Malt for 3 days, cell viability, apoptosis and the expression levels of apoptosis‑associated factors were measured. In addition, the mRNA expression level of miR‑322 was monitored. Furthermore, cells were transfected with an miR‑322 mimic and/or treated with Al‑Malt, and cell viability, apoptosis and the expression levels of apoptosis‑associated factors were measured again. Al‑Malt significantly inhibited cell viability, but promoted apoptosis. The apoptosis‑associated factors, V‑Myc avian myelocytomatosis viral oncogene homolog (c‑Myc), Bcl-2-associated X protein, caspase‑3 and cleaved caspase‑3 were markedly upregulated by Al‑Malt. The mRNA expression level of miR‑322 was negatively regulated by Al‑Malt. Furthermore, miR‑322 attenuated the apoptosis induced by Al‑Malt and recovered the expression changes of these four factors. Thus, miR‑322 may attenuate Al‑Malt‑induced apoptosis by recovering the expression change of c‑Myc. Furthermore, miR‑322 may be involved in the pathogenesis of Al‑Malt‑associated AD. 

Retracted: No

PubPeer comments:
 Fig1.  The changes of cu2011Myc, Bax, caspaseu20113 and cleaved caspaseu20113 expression levels in the cells were measured by (C) western blotting. ![file] Despite the low resolution, the paper s Western Blots bear a generic resemblance to products of the  Tadpole papermill . https: scienceintegritydigest.com 2020 02 21 the-tadpole-paper-mill A typical product: ![] Is it possible to upload or link to higher-resolution scans of the WBs, to dispel any potential criticism? ,
Silencing RBBP6 (Retinoblastoma Binding Protein 6) sensitises breast cancer cells MCF7 to staurosporine and camptothecin-induced cell death
Authors: Pontsho Moela
Lesetja R Motadi
Mpho M S Choene
Journal: Immunobiology (2014)
Discipline: IMMUNOLOGY
Keywords: Apoptosis; Camptothecin; RNA interference; Retinoblastoma Binding Protein 6; Staurosporine.

Abstract:  Retinoblastoma Binding Protein 6 (RBBP6) is a multi-domain protein that uses its ring finger domain to interact with p53 and pRb tumour suppressor genes. The mechanism by which RBBP6 uses to degrade p53 is still unknown; nonetheless it is well known that RBBP6 promotes cell proliferation in several cancers by negatively regulating p53 via its E3 ubiquitin ligase activity. Degradation of p53 by RBBP6 may compromise p53-mediated apoptosis in breast cancer. This study is intended to investigate, the potential applications of RNA interference (RNAi) to block RBBP6 expression, as well as its subsequent effect on cell growth and apoptosis. Our studies indicate that the knockdown of RBBP6 by siRNA modulates p53 gene expression involved in cell death pathways and apoptosis, showing statistically significant gene expression differences. RBBP6 siRNA significantly reduced cell growth compared to the control samples and inhibition of cellular proliferation was observed between 24 and 48h, as shown in the data obtained by real time cell analysis using the xCELLigence system. These results were further confirmed by flow cytometer which showed some apoptotic activity. About 20.7% increase in apoptosis was observed in cells co-treated with RBBP6 siRNA and camptothecin when compared to camptothecin-only whereas in siRBBP6 and staurosporine treated cells there was only an 8.8% increase in apoptosis. These findings suggest that silencing RBBP6 may be a novel strategy to promote camptothecin-induced apoptosis in breast cancer cells. 

Retracted: No

PubPeer comments:
 More similar than expected. Could authors check please? ![file] (A), hypothalamus (B), hippocampus (C), thalamus (D) ,
Immobilization of bioactive fibroblast growth factor-2 into cubic proteinous microcrystals (Bombyx mori cypovirus polyhedra) that are insoluble in a physiological cellular environment
Authors: Akiko Furuyama
Yuriko Nishizaki
Hiroyuki Notsu
Chisa Shukunami
Hajime Mori
Yuji Hiraki
Journal: Journal of Biological Chemistry (2007)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: extracellular matrix; heterotopic signaling cues; fibroblast growth factor-2 (FGF-2); cubic inclusion bodies; Bombyx mori cytoplasmic polyhedrosis virus (BmCPV)
Affiliations: Insect Biomedical Research Center, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto 606-8585, Japan.

Abstract:  The supramolecular architecture of the extracellular matrix and the disposition of its specific accessory molecules give rise to variable heterotopic signaling cues for single cells. Here we have described the successful occlusion of human fibroblast growth factor-2 (FGF-2) into the cubic inclusion bodies (FGF-2 polyhedra) of the Bombyx mori cytoplasmic polyhedrosis virus (BmCPV). The polyhedra are proteinous cubic crystals of several microns in size that are insoluble in the extracellular milieu. Purified FGF-2 polyhedra were found to stimulate proliferation and phosphorylation of p44/p42 mitogen-activated protein kinase in cultured fibroblasts. Moreover, cellular responses were blocked by a synthetic inhibitor of the FGF signaling pathway, SU5402, suggesting that FGF-2 polyhedra indeed act through FGF receptors. Furthermore, FGF-2 polyhedra retained potent growth stimulatory properties even after desiccation. We have demonstrated that BmCPV polyhedra microcrystals that occlude extracellular signaling proteins are a novel and versatile tool that can be employed to analyze cellular behavior at the single cell level. 

Retracted: No

PubPeer comments:
 Blue boxes: Alcian blue staining images of different groups appear to look similar in Fig 4A. ![file] ,
CircRNA circPDSS1 promotes bladder cancer by down-regulating miR-16
Authors: Derong Ma
Pei Liu
Qinnan Yu
Guangye Han
Xiangdong Xue
Journal: Bioscience Reports (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: circPDSS1; miR-16; urothelial bladder cancer.
Affiliations: Department of Urology, The First Affiliated Hospital of Xinxiang Medical College, Weihui City, Henan Province 453100, P.R. China., Department of Urology, Gansu Provincial People's Hospital, Lanzhou City 730000, Gansu Province, P.R. China.

Abstract:  Background: Circular RNA (circRNA) circPDSS1 is a recently identified oncogene in gastric cancer, while its roles in other types of cancer are unknown. We investigated the functions of circPDSS1 in urothelial bladder cancer (UBC). Materials and methods: Seventy-two patients (50 males and 22 females, age 38-69 years, mean: 52.3 ± 6.3 years) with UBC were enrolled in Gansu Provincial People's Hospital from August 2015 to August 2018. RT-qPCR was used to measure gene expression levels in both biopsies from UBC patients and in vitro cultivated HT-1197 and UMUC3 cells. Cell transfections were performed to analyze gene interactions. Cell proliferation, transwell migration and invasion assays were performed to analyze the effects of transfections on HT-1197 and UMUC3 cell proliferation, migration and invasion, respectively. Results: We found that circPDSS1 was up-regulated in UBC. Expression levels of circPDSS1 were increased with increase in clinical stages. MiR-16 was down-regulated and correlated with circPDSS1 in UBC. Overexpression of circPDSS1 led to down-regulation of miR-16, while miR-16 overexpression failed to significantly affect circPDSS1. Overexpression of circPDSS1 led to increased proliferation, invasion and migration rates of UBC cells. Overexpression of miR-16 not only led to inhibited proliferation, invasion and migration of UBC cells, but also attenuated the effects of circPDSS1 overexpression. Conclusion: Therefore, circRNA circPDSS1 may promote UBC by down-regulating miR-16. 

Retracted: No

PubPeer comments:
 Figure 5 seems to have two sets of repeated images. I also wish to note that the email address for the corresponding author does not seem to, um, correspond with their name. *** ![file] , 
  Interestingly, expression levels of miR-16 were **significantly and inversely correlation** with expression levels of circPDSS1 only in tumor tissues (Figure 2B), but not in adjacent healthy tissues (Figure 2C). A minor grammatical error, but an uncommon one. We also find it in [Cheng et al (2019)] :  It was observed that CASC11 and miR-188-5p were **significantly and inversely correlation** in HCC tissues (Figure 3A). In contrast, the correlation between CASC11 and miR-188-5p was not significant in non-cancer tissues (Figure 3B). Perhaps the authors were following a template? I realise that the genre involves strict conventions. ![file] , 
 April 6, 2021 The Editorial Office has been made aware of potential issues surrounding the scientific validity of this paper, hence has issued an expression of concern to notify readers whilst the Editorial Office investigates. ,
Adenocarcinoma at the gastroesophageal junction
Authors: Monika Tripathi
Andrea Grin
Xavier Sagaert
Melissa P Upton
Michael Vieth
Catherine J Streutker
Rupert Langer
Andrew C Chang
Sahar Al-Haddad
Marianna Salemme
Vincenzo Villanacci
Geneviève Soucy
Gert De Hertogh
Journal: Annals of the New York Academy of Sciences (2014)
Discipline: Multidisciplinary
Keywords: Her2; OESO; gastroesophageal junction; immunohistochemistry; intestinal metaplasia
Affiliations: Department of Laboratory Medicine and Pathobiology, St. Michael's Hospital, Toronto, Canada., Section of Thoracic Surgery; University of Michigan Medical Center; Ann Arbor Michigan, Department of Morphology and Molecular Pathology; University Hospitals of K.U. Leuven; Leuven Belgium, St. Michael's Hospital; Toronto Canada, Institute of Pathology; University of Bern; Bern Switzerland, Department of Pathology; Spedali Civili; Brescia Italy, Department of Laboratory Medicine and Pathobiology; St. Michael's Hospital; Toronto Canada, Département de Pathologie - Pathologie Gastro-intestinale; Centre Hospitalier de l'Université de Montréal; Montréal Canada, Department of Cellular Pathology; Oxford University Hospitals NHS Trust; Oxford United Kingdom, Department of Pathology; University of Washington; Seattle Washington, Institute of Pathology; Klinikum Bayreuth; Bayreuth Germany

Abstract:  The following, from the 12th OESO World Conference: Cancers of the Esophagus, includes commentaries on the clinical differences between carcinomas arising slightly above, slightly below, and within the gastroesophageal junction (GEJ); information provided by biopsies; information provided by resection specimens following neoadjuvant therapy; histologic differences existing between carcinomas arising slightly above, slightly below, and within the GEJ; differences provided by immunohistochemistry in these tumors; information given by endoscopic mucosal resection specimens; the role of esophageal pyloric gland adenomas as precursors of adenocarcinomas in the region of the cardia; the role of pancreatic metaplasia; Her2 immunoreactivity to make distinctions in the site of origin; and intestinal metaplasia limited to the cardia as a precursor of adenocarcinoma. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] ,
RETRACTED: Ellipticine-induced apoptosis depends on Akt translocation and signaling in lung epithelial cancer cells
Authors: Hwei-Tien Huang
Kang Fang
Shih-Ping Chen
Chia-Wei Lin
Wan-Chun Cheng
Journal: Lung Cancer (2009)
Discipline: CLINICAL MEDICINE
Keywords: Ellipticine; topoisomerase II inhibitors; antitumor agents; NSCLC; A549 cells
Affiliations: Department of Life Science, National Taiwan Normal University, Taipei, Taiwan. 

Abstract:  Ellipticine and its analogues were reported as topoisomerase II inhibitors and promising antitumor agents. In this work, we showed that the growth of human non-small-cell-lung-cancer (NSCLC) epithelial cells A549 can be inhibited by ellipticine. The inhibitory effect was reverted by PI3K inhibitors. The sub-G(1) phase cells after ellipticine treatment appeared at the expense of those that accumulated first at S- and G(2)/M phases during the early stage of treatment. We showed that the progression leading to cell death was impaired by wortmannin, which reverted apoptosis by retaining cells at S- and G(2)/M transition states. The characteristic apoptosis marker p53 activation after treatment appeared first followed by poly(ADP-ribose)polymerase (PARP) fragmentation. They disappeared upon co-treatment with wortmannin and the apoptotic phenotype reversed. Furthermore, ellipticine regulated endogenous survival signaling by up-regulating phosphorylated Akt that returned to its basal level later. Furthermore, ellipticine induced nucleus translocalization of p53 and Akt and recruitment of autophagosomes. The autophagic-related cell death was interfered by wortmannin and the suppressed growth reverted. The Akt-related cell death also occurred in p53-deficient cells with stable expression of exogenous p53. The work showed that ellipticine-induced cytotoxicity in NSCLC cells was achieved through autophagy and apoptotic death as a result of Akt-modulation. Being a topoisomerase II inhibitor, ellipticine proved a regulator in autophagy-related cell death through corporation of p53 and Akt. 

Retracted: Yes

PubPeer comments:
 October 2016 retraction found here: https: www.lungcancerjournal.info article S0169-5002(16)30451-2 fulltext It reads:  This article has been retracted at the request of the Editor in Chief. Image duplication has been observed within Figure 5A. The authors have been asked to provide an acceptable explanation for this duplication but have not been able to do so neither have the original source files been supplied. Here is the original Figure 5, as reported to the journal in October 2015, with the duplication marked with red boxes. ![file] ,