PReD-Bench/PRed-Bench huggingface dataset:
A positive feedback regulation between long noncoding RNA SNHG1 and YAP1 modulates growth and metastasis in laryngeal squamous cell carcinoma
Authors: Hua Cao
Xiulian Cheng
Ling Gao
Journal: American journal of cancer research (2018)
Discipline: CLINICAL MEDICINE
Keywords: Hippo pathway; YAP1; miR-345.
Affiliations: Department of Otorhinolaryngology, The First Affiliated Hospital of Zhengzhou University Zhengzhou 450052, Henan Province, PR China.

Abstract:  Laryngeal squamous cell carcinoma (LSCC) is the second highest incidence among the head and neck malignancies. Long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) functions as an oncogene in various human cancers. However, the biological functions and molecular mechanisms of SNHG1 in LSCC have not been reported. In this study, we found that lncRNA SNHG1 is significantly upregulated in LSCC and associated with prognosis of LSCC patients. Knockdown of SNHG1 inhibited cell proliferation, migration and invasion and induced cell apoptosis. In addition, knockdown of SNHG1 inhibits LSCC growth and metastasis in vivo. Mechanistically, SNHG1 promotes YAP1 expression and Hippo signaling activity by competitively sponging miR-375. Moreover, YAP1 could occupy the SNHG1 promoter to enhance its transcription, suggesting that there exists a positive feedback regulation between YAP1 and SNHG1. Collectively, our study first elucidates the mechanism of SNHG1-mediated malignant phenotypes through evoking the miR-375/YAP1/Hippo signalling axis, which provides a novel target for LSCC treatment. 

Retracted: Yes

PubPeer comments:
 In Fig. 4, the tumor volume under 100 mm3 is not tumor. Also, measurement at 1-2 weeks is not of tumor, but of the originally injected cells or fibrosis. In C, the sh1 and sh2 group have exactly the same incidence of pulmonary metastasis. In D, of the two animals with metastasis in each group, they each have exactly one animal with one metastasis and one animal with two metastasis. Exactly the same. ![file] In Fig. 5, the bar graphs for the cell line on the left appears to be identical to the one for the cell line on the right. Including identical error bars. ![file] In Fig. 7 C and D, the same situation as Fig. 5. The bars for the left hand cell line appear identical to the bars for the right hand cell line. ![file] , 
 Retracted [1 November 2020] . --------------------------------------------------------------------- Falsified materials and or data reported in this publication had been detected by a knowledgeable reader and subsequently confirmed by further investigation of editorial office. Therefore, the entire article has been retracted in accordance with this journalu2019s policy and editorial decision. ,
MicroRNA-582–3p negatively regulates cell proliferation and cell cycle progression in acute myeloid leukemia by targeting cyclin B2
Authors: Ronghua Xu
Tian Nie
Mao Huang
Paoqiu Wang
Xuefei Tian
Haixia Li
Journal: Cellular & Molecular Biology Letters (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Acute myeloid leukemia; CCNB2; Cell cycle; miR-582–3p.
Affiliations: 1Department of Integrated Chinese and Western Medicine, Hunan Children's Hospital, Changsha, 410007 China., 2Hunan University of Chinese Medicine, Changsha, 410208 China., 3College of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, 410208 China., 4Department of Pediatric Rehabilitation, Hebei Provincial Hospital of Traditional Chinese Medicine, Shijiazhuang, 050000 Hebei China., 5Department of Hematology, The First Hospital of Hunan University of Chinese Medicine, 95 Shaoshan Middle Road, Changsha City, 410007 Hunan Province China.

Abstract:  Background: MicroRNAs (miRNAs) function as post-transcriptional gene expression regulators. Some miRNAs, including the recently discovered miR-582-3p, have been implicated in leukemogenesis. This study aimed to reveal the biological function of miR-582-3p in acute myeloid leukemia (AML), which is one of the most frequently diagnosed hematological malignancies. Methods: The expression of miR-582-3p was determined using quantitative real-time PCR in blood samples from leukemia patients and in cell lines. Cell proliferation and cell cycle distribution were analyzed using the CCK-8, colony formation and flow cytometry assays. The target gene of miR-582-3p was verified using a dual-luciferase reporter assay. The G2/M phase arrest-related molecule contents were measured using western blotting analysis. Results: We found miR-582-3p was significantly downregulated in the blood samples from leukemia patients and in the cell lines. MiR-582-3p overexpression significantly impaired cell proliferation and induced G2/M cell cycle arrest in THP-1 cells. Furthermore, cyclin B2 (CCNB2) was confirmed as a target gene of miR-582-3p and found to be negatively regulated by miR-582-3p overexpression. More importantly, CCNB2 knockdown showed suppressive effects on cell proliferation and cell cycle progression similar to those caused by miR-582-3p overexpression. The inhibitory effects of miR-582-3p overexpression on cell proliferation and cell cycle progression were abrogated by CCNB2 transfection. Conclusion: These findings indicate new functions and mechanisms for miR-582-3p in AML development. Further study could clarify if miR-582-3p and CCNB2 are potential therapeutic targets for the treatment of AML. 

Retracted: No

PubPeer comments:
 Apparent image duplication from another paper from another group. ![file] , 
 ![file] , 
 Apparent image duplication ![file] ,
Exosomal miR-128-3p Promotes Epithelial-to-Mesenchymal Transition in Colorectal Cancer Cells by Targeting FOXO4 via TGF-β/SMAD and JAK/STAT3 Signaling
Authors: Jian Bai
Zhenxian Xiang
Xue Zhang
Yan Fang
Dongdong Shi
Sihao Huang
Jialin Song
Shuyi Wang
Qing Liu
Chaogang Yang
Weisong Zhang
Bin Xiong
Journal: Frontiers in Cell and Developmental Biology (2021)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: EMT; extracellular vesicle; gastrointestinal; microRNA; molecular signaling.
Affiliations: Department of Gastrointestinal Surgery & Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China., Department of Anesthesiology, Peking University Third Hospital, Beijing, China., Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan, China., Hubei Cancer Clinical Study Center, Wuhan, China., Department of General Practice, Beijing Friendship Hospital, Capital Medical University, Beijing, China., Department of Radiation Oncology and Medical Oncology, Zhongnan Hospital of Wuhan University, Wuhan, China.

Abstract:  Epithelial-to-mesenchymal transition (EMT) is a key process that occurs during tumor metastasis, affecting a variety of malignancies including colorectal cancer (CRC). Exosomes mediate cell-cell communication by transporting cell-derived proteins and nucleic acids, including microRNAs (miRNAs). Exosomal delivery of miRNAs plays an important role in tumor initiation, development, and progression. In this study, we investigated the effect of exosomal transfer between CRC cells and aimed to identify specific miRNAs and downstream targets involved in EMT and metastasis in CRC cells. High expression of miR-128-3p was identified in exosomes derived from EMT-induced HCT-116 cells. Altered miR-128-3p expression in CRC cells led to distinct changes in proliferation, migration, invasion, and EMT. Mechanistically, miR-128-3p overexpression downregulated the expression of FOXO4 and induced the activation of TGF-β/SMAD and JAK/STAT3 signaling in CRC cells and xenografted tumors, which led to EMT. Clinically, high expression of miR-128-3p was significantly associated with perineural invasion, lymphovascular invasion, tumor stage, and CA 19-9 content in CRC patients. We revealed that exosomal miR-128-3p regulates EMT by directly suppressing its downstream target gene FOXO4 to activate TGF-β/SMAD and JAK/STAT3 signaling, and the properties of the miR-128-3p/FOXO4 axis were horizontally transferred via exosomal delivery. In turn, exosomal miR-128-3p could be considered as a new therapeutic vehicle for CRC. 

Retracted: No

PubPeer comments:
 Figure 3F and 3G appear to have some images which overlap. *** ![file] , 
 ![file] FIGURE 2 A The original data in the FIGURE 2 A should be derived from another article (PMID: 32679610 ;DOI: 10.1002 1878-0261.12765) after a series of **brightness enhancements**, **flipped images** and **screenshots**. , 
 A large amount of data seems to be shared between the two articles. https: pubpeer.com publications 711F2575DD4D2A3626FE2BFB2FCB76#3 FIGURE 3 F ![file] ,
Adsorption of As(III) and As(V) onto colloidal microparticles of commercial cross-linked polyallylamine (Sevelamer) from single and binary ion solutions
Authors: Margaritis Kostoglou
Dimitrios N Bikiaris
Panoraia I Siafaka
George Z Kyzas
Journal: Journal of Colloid and Interface Science (2016)
Discipline: CHEMISTRY
Keywords: Adsorption; Arsenate; Arsenite; Characterizations; Kinetic modeling
Affiliations: Division of Chemical Technology, Department of Chemistry, Aristotle University of Thessaloniki, GR-541 24 Thessaloniki, Greece., Division of Chemical Technology, Department of Chemistry, Aristotle University of Thessaloniki, GR-541 24 Thessaloniki, Greece. Electronic address: .

Abstract:  This work investigates the removal of arsenic ions in trivalent (As(III)) or pentavalent form (As(V)) from single-component and binary (equal initial ion concentrations) aqueous solutions using commercial cross-linked polyallylamine (namely as Sevelamer) as adsorbent. This is the first work in literature regarding the application of that commercial material as adsorbent for ions. Sevelamer (SVL) is a widely known pharmaceutical compound and the existence of primary and secondary amino groups (with different ratios) in its molecule increases its adsorption potential. For this purpose can be easily proposed as potential sorbent. The adsorption evaluation was based on the pH-effect (optimum pH=6, where As(III) and As(V) removal was 69 and 86%, respectively), isotherms and kinetic curves. The maximum theoretical adsorption capacity (Qm) was 86 and 133mg/g for single-component solutions of As(III) and As(V), respectively. The respective values for binary mixtures of the same concentration (100mg/L) were 84 and 116mg/g, respectively (calculated after fitting to Langmuir-Freundlich isotherm model at 20°C). A novel kinetic interpretation based on the raw experimental kinetics data was also developed. Although adsorption of As(III) and As(V) occurs mainly at different sites, there is an interdependence in their adsorption kinetics. It was found that adsorption from the binary mixtures is a two-stage process. The adsorption mechanism of SVL and arsenic ions interaction was elucidated using FTIR spectroscopy before and after adsorption. SEM images and XRD patterns (the material was amorphous both before and after arsenic adsorption indicating that the mechanism did not alter its physical state) were also taken for the characterization of SVL before and after arsenic adsorption. The adsorption mechanism was mainly attributed to the electrostatic interactions between negatively As ions and positively charged amino groups of SVL. For this reason, As(V) adsorption is higher than As(III). 

Retracted: No

PubPeer comments:
 Figure 2. Four XRD patterns with identical noise ![file] ,
Detecting Borrelia Spirochetes: A Case Study With Validation Among Autopsy Specimens
Authors: Andrew J Dwork
Monica E Embers
Brian A Fallon
Shiva Kumar Goud Gadila
Gorazd Rosoklija
Journal: Frontiers in Neurology (2021)
Discipline: CLINICAL MEDICINE
Keywords: Borrelia; Lewy body; Lyme; PCR; RNA in situ hybridization
Affiliations: Division of Immunology, Tulane National Primate Research Center, Tulane University Health Sciences, Covington, LA, United States., Department of Psychiatry, Columbia University, New York, NY, United States.

Abstract:  The complex etiology of neurodegenerative disease has prompted studies on multiple mechanisms including genetic predisposition, brain biochemistry, immunological responses, and microbial insult. In particular, Lyme disease is often associated with neurocognitive impairment with variable manifestations between patients. We sought to develop methods to reliably detect Borrelia burgdorferi, the spirochete bacteria responsible for Lyme disease, in autopsy specimens of patients with a history of neurocognitive disease. In this report, we describe the use of multiple molecular detection techniques for this pathogen and its application to a case study of a Lyme disease patient. The patient had a history of Lyme disease, was treated with antibiotics, and years later developed chronic symptoms including dementia. The patient's pathology and clinical case description was consistent with Lewy body dementia. B. burgdorferi was identified by PCR in several CNS tissues and by immunofluorescent staining in the spinal cord. These studies offer proof of the principle that persistent infection with the Lyme disease spirochete may have lingering consequences on the CNS. 

Retracted: No

PubPeer comments:
 Criticised in  Lack of Convincing Evidence that Borrelia burgdorferi Infection Causes Either Alzheimeru2019s Disease or Lewy Body Dementia (Wormser et al 2021). https: lymescience.org wp-content uploads 2021 12 Lack-of-Convincing-Evidence-that-Borrelia-burgdorferi-Infection-Causes-Either-Alzheimers-Disease-or-Lewy-Body-Dementia.pdf https: twitter.com LymeScience status 1466426870556151811 ,
L. plantarum prevents enteroinvasive Escherichia coli-induced tight junction proteins changes in intestinal epithelial cells
Authors: Huanlong Qin
Yanqun Jiang
Xiaomin Hang
Zhongwei Zhang
Journal: BMC Microbiology (2009)
Discipline: MICROBIOLOGY
Keywords: Lactobacillus plantarum; Enteropathogenic Escherichia coli; epithelial monolayer barrier function; host cell morphology; attaching/effacing lesion
Affiliations: Department of Surgery, Affiliated Sixth People's Hospital, Shanghai Jiao Tong University, Shanghai 200233, PR China. 

Abstract:  Background: It is increasingly recognized that Lactobacillus plantarum (L. plantarum) has the ability to protect against Enteropathogenic Escherichia coli (EPEC)-induced damage of the epithelial monolayer barrier function by preventing changes in host cell morphology, attaching/effacing (A/E) lesion formation, monolayer resistance, and macromolecular permeability. However, the cellular mechanism involved in this protective effect still remained to be clarified. Methods: This study was to investigate the effect of L. plantarum on the changes of Caco-2 cells responding to Enteroinvasive Escherichia coli (EIEC), the permeability of cell monolayer and the transmissivity of dextran, and the distribution and expression of the tight junction (TJ) proteins, such as Claudin-1, Occludin, JAM-1 and ZO-1 were examined when infected with EIEC or adhesived of L. plantarum after infection by confocal laser scanning microscopy (CLSM), immunohistochemistry and Western blotting, the cytoskeleton protein F-actin were observed with FITC-phalloidin. Results: This study demonstrated that the transepithelial electrical resistance (TER) step down and dextran integrated intensity (DII) step up with time after infected with EIEC, but after treating with L. plantarum, the changes of TER and DII were improved as compared with EIEC group. L. plantarum prevented the damage of expression and rearrangement of Claudin-1, Occludin, JAM-1 and ZO-1 proteins induced by EIEC, and could ameliorate the injury of cytoskeleton protein F-actin infected with EIEC. Conclusion: L. plantarum exerted a protective effect against the damage to integrity of Caco-2 monolayer cells and the structure and distribution of TJ proteins by EIEC infection. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. , 
 I agree with the finding above. I actually already had found this by eye, and reported it to the journal in July 2015, but no action so far. ,
Polyamine depletion increases cytoplasmic levels of RNA-binding protein HuR leading to stabilization of nucleophosmin and p53 mRNAs
Authors: Tongtong Zou
Myriam Gorospe
Lan Liu
Krystyna Mazan-Mamczarz
Bernard S Marasa
Ai-Hong Zhang
Lan Xiao
Jaladanki N Rao
Rudolf Pullmann
Jian-Ying Wang
Journal: Journal of Biological Chemistry (2006)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Polyamines; HuR; NPM; p53; mRNA stability
Affiliations: Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore 21201, USA.

Abstract:  Polyamines are essential for maintaining normal intestinal epithelial integrity, an effect that relies, at least in part, on their ability to keep low levels of nucleophosmin (NPM) and p53 mRNAs. The RNA-binding protein HuR associates with the p53 mRNA, as reported previously, and with the NPM mRNA, computationally predicted to be a target of HuR. Here, we show that HuR binds the NPM and p53 3'-untranslated regions and stabilizes these mRNAs in polyamine-depleted intestinal epithelial cells. Depletion of cellular polyamines by inhibiting ornithine decarboxylase with alpha-difluoromethylornithine dramatically enhanced the cytoplasmic abundance of HuR, whereas ectopic ornithine decarboxylase overexpression decreased cytoplasmic HuR; neither intervention changed whole-cell HuR levels. HuR was found to specifically bind the 3'-untranslated regions of NPN and p53 mRNAs. HuR silencing rendered the NPM and p53 mRNAs unstable and prevented increases in NPM and p53 mRNA and protein in polyamine-deficient cells. These results indicate that polyamines modulate cytoplasmic HuR levels in intestinal epithelial cells, in turn controlling the stability of the NPM and p53 mRNAs and influencing NPM and p53 protein levels. 

Retracted: No

PubPeer comments:
 ![file] There are multiple undeclared splicing sites in the immunoblots in Figure 4B ,
Differential modification of p27Kip1 controls its cyclin D-cdk4 inhibitory activity
Authors: Dina Leznova
Arpita Ray
Stacy W Blain
Melissa K James
Journal: Molecular and Cellular Biology (2008)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: p27; cyclin D-cdk4/6 inhibitor; two-state mechanism; tyrosine phosphorylation; growth-state-dependent
Affiliations: Department of Pediatrics, SUNY Downstate Medical Center, 450 Clarkson Ave., Box 49, Brooklyn, NY 11203, USA. 

Abstract:  Whether p27 is a cyclin D-cdk4/6 inhibitor or not is controversial, and how it might switch between these two modes is unknown. Arguing for a two-state mechanism, we show that p27 bound to cyclin D-cdk4 can be both inhibitory and noninhibitory, due to its differential-growth-state-dependent tyrosine phosphorylation. We found that p27 from proliferating cells was noninhibitory but that p27 from arrested cells was inhibitory, and the transition from a bound noninhibitor to a bound inhibitor was not due to an increase in p27 concentration. Rather, two tyrosine residues (Y88 and Y89) in p27's cdk interaction domain were phosphorylated preferentially in proliferating cells, which converted p27 to a noninhibitor. Concordantly, mutation of these sites rendered p27 resistant to phosphorylation and locked it into the bound-inhibitor mode in vivo and in vitro. Y88 was directly phosphorylated in vitro by the tyrosine kinase Abl, which converted p27 to a cdk4-bound noninhibitor. These data show that the growth-state-dependent tyrosine phosphorylation of p27 modulates its inhibitory activity in vivo. 

Retracted: No

PubPeer comments:
 ![file] , 
 ![file] , 
 Additional problematic data figure 3A. https: imgur.com iSMo18A , 
 Figure 4D. https: imgur.com wjpeGVf , 
 Figure 4B. Vertical mirror image and partial mirror image. https: imgur.com 50hEpjR , 
 ![file] , 
 ![file] , 
 Figure 5. https: imgur.com PbNOEPx , 
 #1 Figure 1G continued. https: imgur.com jTCadhg , 
 22 Aug 2022 Expression of Concern. https: journals.asm.org doi 10.1128 mcb.00323-22 The American Society for Microbiology (ASM) and Molecular and Cellular Biology (MCB) are issuing this Expression of Concern regarding the following publication: James MK, Ray A, Leznova D, Blain SW. 2008. Differential modification of p27Kip1 controls its cyclin D-cdk4 inhibitory activity. Mol Cell Biol 28:498u2013510. https: doi.org 10.1128 MCB.02171-06. Molecular and Cellular Biology was notified that the above-mentioned paper was investigated by the SUNY Downstate Health Sciences University and that potential image duplications were found in Fig. 3A and 6B. This Expression of Concern is issued pending the outcome of ongoing litigation between SUNY Downstate Health Sciences University and the corresponding author of the paper, Stacy Blain, in the United States. District Court of the Eastern District of New York. , 
 #10 https: ia802504.us.archive.org 22 items gov.uscourts.nyed.480260 gov.uscourts.nyed.480260.1.0.pdf , 
 https: retractionwatch.com 2022 08 25 exclusive-cancer-researcher-sues-med-school-for-retaliation-after-research-misconduct-finding ,
PI3-kinase/Akt is constitutively active in primary acute myeloid leukaemia cells and regulates survival and chemoresistance via NF-kappaB, Mapkinase and p53 pathways
Authors: V L Grandage
A Khwaja
D C Linch
R E Gale
Journal: Leukemia (2005)
Discipline: CLINICAL MEDICINE
Keywords: PI3-kinase; Akt; AML; cell survival; proliferation
Affiliations: Royal Free and University College London Medical School, Department of Haematology, 98 Chenies Mews, London, UK. 

Abstract:  The phosphoinositide 3-kinase (PI3-kinase) signalling pathway plays a key role in the regulation of cell survival and proliferation. We show that the PI3-kinase/Akt pathway is constitutively active in primary acute myeloid leukaemia (AML) cells and that blockade by the selective inhibitor LY294002 reduces survival of the total blast population (mean 52%). The ERK/MAPK module is also constitutively active and treatment with the MAPKK inhibitor U0126 reduces cell survival by 22%. In 10 of 18 samples, PI3-kinase contributes to MAPK activation as incubation with LY294002 leads to a marked reduction in its phosphorylation. PI3-kinase inhibition reduces survival of the CD34+38- AML progenitor subset by 44%, whereas MAPKK inhibition has little effect. Reporter assays in primary AML cells show that blocking PI3-kinase leads to a marked reduction of constitutive NF-kappaB activity and promotes p53-mediated transcription. This is associated with a synergistic interaction between LY294002 and Ara-C. An inducible activated form of Akt protects normal myeloid cells from Ara-C and etoposide-mediated apoptosis. These results show that blocking PI3-kinase has direct antileukaemic effects and potentiates the response to conventional cytotoxics via a number of targets including NF-kappaB, p53 and MAPK. Inhibitors of PI3-kinase and Akt may be useful in the treatment of AML. 

Retracted: No

PubPeer comments:
 Figure 1. * Red boxes: The a-tubulin panels in a) look unexpectedly similar to thee b-tubulin panels in c). Part of a set of 60+ papers reported to the journal in October 2015 with a friendly reminder in 2017. In the past five years, the journal did not correct or retract a single paper from this set. ![file] ,
MicroRNA‑758 inhibits malignant progression of retinoblastoma by directly targeting PAX6
Authors: Xinying You
Jun Li
Journal: Oncology Reports (2018)
Discipline: CLINICAL MEDICINE
Keywords: miRNA-758; retinoblastoma; tumourigenesis; tumour development; therapeutic methods
Affiliations: Department of Ophthalmology, Liaocheng People's Hospital, Liaocheng, Shandong 252000, P.R. China.

Abstract:  Accumulated studies have highlighted that the dysregulation of microRNAs (miRNAs) in retinoblastoma (RB) is a leading cause for tumourigenesis and tumour development. Therefore, the elucidation of the expression, functional roles and underlying mechanisms of miRNAs in RB will help the development of promising therapeutic methods to improve the prognosis of RB patients. The aim of this study was to detect miRNA‑758 (miR‑758) expression in RB tissues and cell lines, and to determine the effects and underlying mechanisms of miR‑758 on RB progression. The results demonstrated that miR‑758 was downregulated in both RB tissues and cell lines. In vitro functional experiments revealed that upregulation of miR‑758 inhibited cell proliferation, migration and invasion, and induced apoptosis in RB. In addition, paired box protein 6 (PAX6) was a direct target gene of miR‑758 in RB. Furthermore, PAX6 was upregulated in RB tissues, and this upregulation was inversely associated with the expression level of miR‑758. In addition, PAX6 reintroduction abrogated the tumour‑suppressive effects of miR‑758 overexpression on RB cell proliferation, migration, invasion and apoptosis. Furthermore, miR‑758 overexpression inactivated the PI3K/Akt pathway in RB cells by inhibiting PAX6. In conclusion, our current study provided sufficient evidence to demonstrate that miR‑758 inhibits the progression of RB by directly targeting PAX6 and regulating the PI3K/Akt pathway, thereby suggesting that this miRNA may be developed as a therapeutic target for treating patients with RB. 

Retracted: No

PubPeer comments:
 Figs 2D, 6D.  The apoptosis rate in Y79 and WERI-RB1 cells transfected with miR-758 mimics or miR-NC was evaluated using a flow cytometric assay ;  Cell ... apoptosis in the aforementioned cells were evaluated using... flow cytometric assays . ![file] Panel marked with bright pink box also appears in Fig 6H of [Dai et al (2020)] . ![] Here in context: ![] -------------------------------------- Panel marked with lavender rectangle also appears in Figs 6H of Dai et al, and in 2D, 4D, 5D of [Zhang et al (2019)] .  The apoptosis rate of H522 and H460 cells transfected with miR-802 mimics or miR-NC was assessed via Annexin V and PI staining ;  Annexin V and PI staining was used to detect the apoptosis rate of H522 and H460 cells following FGFR1 silencing ;  apoptosis ... of the aforementioned cells were assayed . ![] ![file] ,
Lack of effect of dexamethasone on growth of Orientia tsutsugamushi Gilliam in mouse L929 cells
Authors: Su Jin Jeong
Young Goo Song
Ae Jung Huh
June Myung Kim
Sang Hoon Han
Joon Sup Yeom
Jun Yong Choi
Bum Sik Chin
Kkot Sil Lee
Chang Oh Kim
Journal: Yonsei Medical Journal (2011)
Discipline: CLINICAL MEDICINE
Keywords: corticosteroid; rickettsial disease; Orientia tsutsugamushi; growth; in vitro
Affiliations: Department of Internal Medicine, Yonsei University College of Medicine, 250 Seongsan-ro, Seodaemun-gu, Seoul 120-752, Korea., Department of Internal Medicine, National Health Insurance Corporation Ilsan Hospital, Goyang, Korea., Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea., Department of Internal Medicine, Kwandong University Myongji Hospital, Kwandong University College of Medicine, Goyang, Korea., Department of Internal Medicine and AIDS Research Institute, Yonsei University College of Medicine, Seoul, Korea.

Abstract:  Purpose: Previous studies and our own clinical experience suggest that concurrent corticosteroid treatment for severe rickettsial disease with multiorgan failure may improve the clinical course or reduce mortality. However, the use of corticosteroids as adjunctive treatment for rickettsial diseases is controversial. We attempted to determine the influences of corticosteroid on the growth of Orientia tsutsugamushi in vitro to justify and evaluate the clinical applicability of corticosteroid in rickettsial disease. Materials and methods: L929 cells were infected with Orientia tsutsugamushi Gilliam. Dexamethasone was added to the cells at final concentrations of 10¹ and 10⁷ pg/mL. Cultures were incubated at 35°C and processed for flow cytometry on the 6th day after addition of dexamethasone. Results: Observation on the 6th day after treatment with dexamethasone in infected cultures revealed that there was no difference in fluorescence intensity among the treatment wells. Treatment of the cells with dexamethasone at concentrations of 10¹ and 10⁷ pg/mL showed no influence on the growth of Orientia tsutsugamushi. Conclusion: Our results to show that isolated corticosteroid does not enhance the replication of Orientia tsutsugamushi in vitro. Concurrent use of anti-inflammatory or immunosuppressive doses of corticosteroids in conjunction with antibiotics may not have detrimental effects on the course of scrub typhus. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
LncRNA-MALAT1 regulates proliferation and apoptosis of ovarian cancer cells by targeting miR-503-5p
Authors: Fangfang Xie
Qian Li
Qian Sun
Journal: OncoTargets and Therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: JAK2/STAT3; cell apoptosis; cell proliferation; lncRNA-MALAT1; miR-503-5p
Affiliations: Department of Obstetrics and Gynecology, The 940th Hospital of Joint Logistics Support Force of Chinese People's Liberation Army, Lanzhou, Gansu 730050, People's Republic of China.

Abstract:  Objective: Ovarian cancer (OC) is a common female disease with a poor prognosis. But the possible mechanism of OC tumor progression remains an active area of research. This study is intended to explore the effect of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on proliferation and apoptosis of OC and its mechanism. Materials and methods: MALAT1 and miR-503-5p expressions in human OC cell lines and normal human ovarian epithelial (HOSE) cell line were measured using qRT-PCR. OC cell line SKOV3 is divided into 4 groups: pcDNA3.1 group, pcDNA3.1-MALAT1 group, si-NC group, and si-MALAT1 group. MTT assay and 5-ethynyl-2'-deoxyuridine (EdU) assay were applied for the detection of cell proliferation. Relationship of MALAT1 with miR-503-5p was verified using luciferase assay and RNA pull-down. The luciferase activity in cells was normalized to RNA concentrations determined by Bradford assays. Results: MALAT1 expression in OC cells was elevated compared with HOSE cells. MTT assay and EdU assay supported that si-MALAT1 could inhibit cell proliferation in OC cells. Treatment of si-MALAT1 results in increased cell apoptosis rate in both SKOV3 cells and OVCAR3 cells. The expression of lncRNA-MALAT1 was negatively associated with the expression of miR-503-5p in OC cells, while luciferase assay and RNA pull-down together supported the direct binding of MALAT1 with miR-503-5p. Knockdown of MALAT1 was able to inhibit the activation of JAK2/STAT3 signal pathway, and MALAT1 overexpression was accompanied by activation of these factors. Conclusion: lncRNA-MALAT1 can negatively target miR-503-5p expression to further promote proliferation and depress apoptosis of OC cells through the JAK2-STAT3 pathway. 

Retracted: No

PubPeer comments:
 There are numerous repeated patterns between (as below) ![file] and within (below) ![file] panels purporting to show results of flow cytometry analyses. I struggle to find an innoccuous explanation for these. ,
Alpha-synuclein up-regulation and aggregation during MPP+-induced apoptosis in neuroblastoma cells: intermediacy of transferrin receptor iron and hydrogen peroxide
Authors: Joy Joseph
Srigiridhar Kotamraju
Cecilia J Hillard
Shasi V Kalivendi
Sonya Cunningham
B Kalyanaraman
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MPP(+); neurotoxin; Parkinson's disease; iron; transferrin receptor
Affiliations: Department of Biophysics and Free Radical Research Center, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.

Abstract:  1-Methyl-4-phenylpyridinium (MPP(+)) is a neurotoxin that causes Parkinson's disease in experimental animals and humans. Despite the fact that intracellular iron was shown to be crucial for MPP(+)-induced apoptotic cell death, the molecular mechanisms for the iron requirement remain unclear. We investigated the role of transferrin receptor (TfR) and iron in modulating the expression of alpha-synuclein (alpha-syn) in MPP(+)-induced oxidative stress and apoptosis. Results show that MPP(+) inhibits mitochondrial complex-1 and aconitase activities leading to enhanced H(2)O(2) generation, TfR expression and alpha-syn expression/aggregation. Pretreatment with cell-permeable iron chelators, TfR antibody (that inhibits TfR-mediated iron uptake), or transfection with glutathione peroxidase (GPx1) enzyme inhibits intracellular oxidant generation, alpha-syn expression/aggregation, and apoptotic signaling as measured by caspase-3 activation. Cells overexpressing alpha-syn exacerbated MPP(+) toxicity, whereas antisense alpha-syn treatment totally abrogated MPP(+)-induced apoptosis in neuroblastoma cells without affecting oxidant generation. The increased cytotoxic effects of alpha-syn in MPP(+)-treated cells were attributed to inhibition of mitogen-activated protein kinase and proteasomal function. We conclude that MPP(+)-induced iron signaling is responsible for intracellular oxidant generation, alpha-syn expression, proteasomal dysfunction, and apoptosis. Relevance to Parkinson's disease is discussed. 

Retracted: No

PubPeer comments:
 ![file] ,
Nano-fibre Integrated Microcapsules: A Nano-in-Micro Platform for 3D Cell Culture
Authors: Jeffrey M Macdonald
Shalil Khanal
Narayan Bhattarai
Jagannathan Sankar
Shanta R Bhattarai
Ramji K Bhandari
Journal: Scientific Reports (2019)
Discipline: Multidisciplinary
Keywords: NIM system; polymeric nanofibre-integrated alginate; PNA hydrogel microcapsules; cryo-ground poly (lactide-co-glycolide) nanofibres; CPN
Affiliations: Department of Applied Science and Technology, North Carolina A&T State University, Greensboro, NC, USA., Department of Chemical, Biological, and Bioengineering, North Carolina A&T State University, Greensboro, NC, USA., Department of Chemistry, North Carolina A&T State University, Greensboro, NC, USA., Department of Biology, North Carolina A&T State University, Greensboro, NC, USA., Department of Biology, University of North Carolina Greensboro, Greensboro, NC, USA., Department of Mechanical Engineering, North Carolina A&T State University, Greensboro, NC, USA., Department of Biomedical Engineering, University of North Carolina, Chapel Hill, NC, USA., Department of Chemical, Biological, and Bioengineering, North Carolina A&T State University, Greensboro, NC, USA. .

Abstract:  Nano-in-micro (NIM) system is a promising approach to enhance the performance of devices for a wide range of applications in disease treatment and tissue regeneration. In this study, polymeric nanofibre-integrated alginate (PNA) hydrogel microcapsules were designed using NIM technology. Various ratios of cryo-ground poly (lactide-co-glycolide) (PLGA) nanofibres (CPN) were incorporated into PNA hydrogel microcapsule. Electrostatic encapsulation method was used to incorporate living cells into the PNA microcapsules (~500 µm diameter). Human liver carcinoma cells, HepG2, were encapsulated into the microcapsules and their physio-chemical properties were studied. Morphology, stability, and chemical composition of the PNA microcapsules were analysed by light microscopy, fluorescent microscopy, scanning electron microscopy (SEM), Fourier-Transform Infrared spectroscopy (FTIR), and thermogravimetric analysis (TGA). The incorporation of CPN caused no significant changes in the morphology, size, and chemical structure of PNA microcapsules in cell culture media. Among four PNA microcapsule products (PNA-0, PNA-10, PNA-30, and PNA-50 with size 489 ± 31 µm, 480 ± 40 µm, 473 ± 51 µm and 464 ± 35 µm, respectively), PNA-10 showed overall suitability for HepG2 growth with high cellular metabolic activity, indicating that the 3D PNA-10 microcapsule could be suitable to maintain better vitality and liver-specific metabolic functions. Overall, this novel design of PNA microcapsule and the one-step method of cell encapsulation can be a versatile 3D NIM system for spontaneous generation of organoids with in vivo like tissue architectures, and the system can be useful for numerous biomedical applications, especially for liver tissue engineering, cell preservation, and drug toxicity study. 

Retracted: No

PubPeer comments:
 In Figure 5, two micrographs have been dupcliated and presented as something else. ![file] ,
Solution Grown Single-Unit-Cell Quantum Wires Affording Self-Powered Solar-Blind UV Photodetectors with Ultrahigh Selectivity and Sensitivity
Authors: Xiaohong Li
Simeng Hao
Louzhen Fan
Guanjie Xing
Dong Li
Yunchao Li
Shihe Yang
Journal: Journal of the American Chemical Society (2019)
Discipline: CHEMISTRY
Keywords: semiconductor nanowires; single-unit-cell thickness; soft template; oriented attachment; ZnS
Affiliations: College of Chemistry , Beijing Normal University , Beijing 100875 , China., Guangdong Key Lab of Nano-Micro Material Research, School of Chemical Biology and Biotechnology, Shenzhen Graduate School , Peking University , Shenzhen 518055 , China.

Abstract:  As crystalline semiconductor nanowires are thinned down to a single-unit-cell thickness, many fascinating properties could arise pointing to promising applications in various fields. A grand challenge is to be able to controllably synthesize such ultrathin nanowires. Herein, we report a strategy, which synergizes a soft template with oriented attachment (ST-OA), to prepare high-quality single-unit-cell semiconductor nanowires (SSNWs). Using this protocol, we are able to synthesize for the first time ZnS and ZnSe nanowires (NWs) with only a single-unit-cell thickness (less than 1.0 nm) and a cluster-like absorption feature (i.e., with a sharp, strong, and significantly blue-shifted absorption peak). Particularly, the growth mechanism and the single-unit-cell structure of the as-prepared ZnS SSNWs are firmly established by both experimental observations and theoretical calculations. Thanks to falling into the extreme quantum confinement regime, these NWs are found to only absorb the light with wavelengths shorter than 280 nm (i.e., solar-blind UV absorption). Utilizing such a unique property, self-powered photoelectrochemical-type photodetectors (PEC PDs) based on the ZnS SSNWs are successfully fabricated. The PDs after interface modification with TiO2 exhibit an excellent solar-blind UV photoresponse performance, with a typical on/off ratio of 6008, a detectivity of 1.5 × 1012 Jones, and a responsivity of 33.7 mA/W. This work opens the door to synthesizing and investigating a new dimension of nanomaterials with a wide range of applications. 

Retracted: No

PubPeer comments:
 The author appears to have confused whether albino mice or rats were the subject of this study. Could you please clarify this point? ![file] ,
Splicing regulator SC35 is essential for genomic stability and cell proliferation during mammalian organogenesis
Authors: Xue Li
Ye Sun
Michael G Rosenfeld
Jian-Hua Ding
Shengrong Lin
Xiang-Dong Fu
Ran Xiao
Dave W Rose
Journal: Molecular and Cellular Biology (2007)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: SR family; splicing regulators; gene expression; SC35; cell proliferation
Affiliations: Department of Surgery/Urology, Children's Hospital of Boston, Harvard Medical School, 300 Longwood Ave., Boston, MA 02115, USA.

Abstract:  The members of the SR family of splicing regulators were initially characterized for their critical roles in constitutive and regulated splicing. They are implicated in different aspects of gene expression processes, including transcription, RNA stability, mRNA transport, and translational control. While knockout studies have demonstrated their essential functions during animal development, the pathway(s) leading to a specific cellular phenotype remains poorly understood. We report here that the SR protein SC35 controls cell proliferation during pituitary gland development but is completely dispensable in terminal differentiated mature cardiomyocytes in mice. We show that loss of SC35 in mouse embryonic fibroblasts induces G2/M cell cycle arrest and genomic instability, resulting at least in part from p53 hyperphosphorylation and hyperacetylation. While p53 hyperphosphorylation appears related to ATM activation, its hyperacetylation has been attributed to the increased expression of the acetyltransferase gene p300 and the aberrant splicing of the deacetylase gene SirT1. These findings reveal the involvement of SC35 in specific pathways in regulating cell proliferation and genomic stability during mammalian organogenesis and suggest its potential function in tumorigenesis. 

Retracted: No

PubPeer comments:
 In Figure 7C, acK317 and p53 total showed unexpected similarities. Please explain. ![file] ,
ERCC6L that is up-regulated in high grade of renal cell carcinoma enhances cell viability in vitro and promotes tumor growth in vivo potentially through modulating MAPK signalling pathway
Authors: Chengcheng Lv
Zi Yu
Chuize Kong
Yu Zeng
Gejun Zhang
Shui Fu
Cheng Fu
Qingzhuo Dong
Journal: Cancer Gene Therapy (2019)
Discipline: CLINICAL MEDICINE
Keywords: Renal cell carcinoma; ERCC6L; gene expression; cell viability; apoptosis
Affiliations: Department of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning, 110042, China., Department of Urology, The First Hospital of China Medical University, Shenyang, Liaoning, 110001, China., Department of Urology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning, 110042, China. .

Abstract:  Renal cell carcinoma (RCC), which is one of the most diagnosed urological malignancies worldwide, is usually associated with abnormality in both genetic and cellular processes. In the present study, through analyzing The Cancer Genome Atlas (TCGA) dataset, we screened out ERCC6L as a candidate gene that is potentially related to the development of RCC based on its increased expression in ccRCC tissues compared with normal kidney tissues as well as its possible relevance to cancer prognosis. Evidence indicates that ERCC6L is an indispensable component of mammalian cell mitosis, while it fails to disclose the role of ERCC6L in tumorigenesis. By using RT-PCR, it was confirmed that the mRNA expression of ERCC6L was upregulated in RCC tissues as compared to normal controls in 28 pared samples. In addition, the immunohistochemistry study in a tissue microarray (TMA) containing 150 ccRCC samples showed that the staining score of ERCC6L was positively correlated with the Fuhrman grade of cancers. Next, when the expression of ERCC6L was lowered by specific shRNA, the cell viability was significantly inhibited in 786-O and Caki-1 cells, while the apoptosis was induced accordingly. At the same time, RCC cells those were transfected with shRNA targeting to ERCC6L grew significantly slower than parental cells in immunodeficient mice. These results consistently suggest that ERCC6L may play a role in regulating the cell viability of RCC both in vitro and in vivo. Further, gene expression microarray analysis followed by the validating western blot after knocking down ERCC6L expression in 786-O cells highlighted the involvement of MAPK signaling pathway in regulation of ERCC6L on cellular process of RCC. In conclusion, the present study suggests a likely promoting role of ERCC6L on the development of RCC. Thus, further study to explore the potential utility of ERCC6L as a novel therapeutic target of RCC is clearly needed. 

Retracted: No

PubPeer comments:
 Figure 2G: The flow cytometry data of Annexin V staining is surprisingly similar between two different cell lines, both for sh-ctrl and sh-ERCC6L. Figure 3A: The fluorescence micrograph presented for  null is empty. Even if you enhance the contrast to the extreme, there is no background signal. ![file] ,
Melanoma Unknown Primary Brain Metastasis Treatment with ECHO-7 Oncolytic Virus Rigvir: A Case Report
Authors: Agnija Rasa
Guna Proboka
Pēteris Alberts
Sergejs Isajevs
Andra Tilgase
Journal: Frontiers in Oncology (2018)
Discipline: CLINICAL MEDICINE
Keywords: ECHO-7 virus; Rigvir®; blood–brain barrier; intranasal; melanoma brain metastasis
Affiliations: Latvian Oncology Centre, Riga Eastern Clinical University Hospital, Riga, Latvia., R&D, International Virotherapy Center, Riga, Latvia., Department of Pathology, Riga Eastern Clinical University Hospital, Riga, Latvia., Department of Pathology, Faculty of Medicine, University of Latvia, Riga, Latvia.

Abstract:  Melanoma is considered an aggressive malignancy with a tendency of forming metastasis in the brain. Less than 10% of all melanoma cases present with unknown primary tumor location. This diagnose is yet to be fully understood, because there are only theoretical assumptions about the nature of the disease. Melanoma brain metastases have many severe side effects and, unfortunately, any disease related to the brain has limited therapeutic options due to the blood-brain barrier. The course of the disease after a treatment course is complicated to predict, and it is difficult to obtain long-lasting remission. In this report, we describe a female patient with unknown primary melanoma brain metastasis treated with the oncolytic ECHO-7 virus Rigvir® after brain surgery. The patient has been stable, as monitored by magnetic resonance imaging, for more than 3.8 years with ongoing therapy. The median expected overall survival from the time of diagnosis is approximately 5 months. Additional positive effect could have been gained from use of the intranasal administration route, which is considered effective due to the direct anatomical connection between the nasal cavity and the central nervous system. However, further studies are required to fully understand this mode of drug administration. 

Retracted: No

PubPeer comments:
 Now that the Latvian government has withdrawn support for Rigvir , would the publishers like to reconsider this advertisement they accepted for a product reported to be fake? https: eng.lsm.lv article society society institution-asks-rigvir-to-repay-state-funds-used-for-botched-drug-batch.a315108 https: eng.lsm.lv article society health rigvir-cancer-treatment-at-center-of-fresh-controversy.a313826 ,