PReD-Bench/PRed-Bench huggingface dataset:
Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway
Authors: Zhuo-Xun Wu
Wei Guo
Lanting Tao
Haiyan Du
Zhe-Sheng Chen
Jing Wang
Lingling Sun
Lizhu Lin
Jue Zhang
Hanrui Chen
Xiaozhong Liao
Journal: Frontiers in Oncology (2020)
Discipline: CLINICAL MEDICINE
Keywords: A549; PC9; VEGF/PI3K/Akt signal pathway; apatinib; cordycepin
Affiliations: Department of Oncology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China., Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY, United States., Department of Biochemistry, Guangzhou University of Chinese Medicine, Guangzhou, China.

Abstract:  Background: The application of apatinib is immensely limited by its acquired drug resistance. This research investigates whether cordycepin, a component from Cordyceps could synergize with apatinib to improve its anticancer effect on non-small cell lung cancer (NSCLC) cells. Methods: The NSCLC cell lines A549, PC9, and H1993, and human bronchial epithelial (HBE) cell line Bears-2B were used in this study. Cell counting kit 8, colony formation assays, wound healing assay, transwell assay, and flow cytometry analysis were performed to assess the cell viability, the migration ability, and invasion ability of the cells. Kyoto encyclopedia of genes and genomes (KEGG), western blotting and molecular docking was applied to analyze the possible pathways affected by cordycepin. Results: The combination of cordycepin and apatinib in a ratio of 5:1 synergistically reduced proliferation of NSCLC cells, inhibited cell migration and invasion, increased cell apoptosis by altering cell cycle in NSCLC A549 and PC9 cells. The VEGF/PI3K/Akt pathway was inhibited after treatment with cordycepin and apatinib. Conclusion: Our findings demonstrated that the combination of cordycepin and apatinib has synergistically anticancer effect on NSCLC cells by down-regulating VEGF/PI3K/Akt signaling pathway. This result indicated that cordycepin and apatinib could be a promising drug combination against NSCLC. 

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. *** ![file] ,
RETRACTED ARTICLE: Tumor suppressor microRNA-31 inhibits gastric carcinogenesis by targeting Smad4 and SGPP2
Authors: H Jisheng
Y Zhen
Z Tengteng
W Ruoming
Journal: Cancer Gene Therapy (2015)
Discipline: CLINICAL MEDICINE
Keywords: microRNA-31; gastric cancer; pathogenesis; SGPP2; Smad4
Affiliations: General Surgery of First Renmin Hospital of Shangqiu, Zhengzhou, China., Gastrointestinal Surgery of First Affiliated Hospital of Zhengzhou University, Zhengzhou, China., Cancer Department of First Renmin Hospital of Shangqiu, Zhengzhou, China.

Abstract:  To investigate the function of microRNA-31 (miR-31) in the pathogenesis of gastric cancer (GC) and to explore the possible mechanisms involved in it. A quantitative real-time reverse transcription-PCR (RT-PCR) analysis was performed to evaluate miR-31 expression in GC cell lines. After transfecting GC cells with miR-31 precursors, Alamar blue and apoptosis assays were used to measure the respective proliferation and apoptosis rates. SGPP2 and Smad4 expression were determined by real-time RT-PCR and western blot assays after miR-31 transfection. Animal assay was used to further investigate miR-31 in the pathogenesis of GC. miR-31 was significantly reduced in GC tissues and GC cell lines, and that the reduced miR-31 was associated with distant metastasis and GC clinical pathological stages, miR-31 was lower at stages III/IV than that at stage II. SGPP2 and Smad4 were proven to be the direct target of miR-31. SGPP2 and Smad4 at mRNA and protein levels were negatively correlated with miR-31 in human GC tissues and cancer cell lines. Increased miR-31 significantly repressed SGPP2 and Smad4 at transcriptional and translational levels. Functional studies showed that increasing miR-31 inhibited GC cell proliferation, promoted apoptosis and attenuated cell migration, which were also linked to downregulation of STAT3. In vivo, miR-31 inhibited GC cell growth in tumor-bearing mice. This study has revealed miR-31 as a tumor suppressor and has identified SGPP2 and Smad4 as novel targets of miR-31, linking to STAT3 for regulating cancer cell proliferation, apoptosis and migration in GC. Therefore, miR-31 could be a useful biomarker for monitoring GC development and progression, and also could have a therapeutic potential by targeting SGPP2, Smad4 and STAT3 for GC therapy. 

Retracted: Yes

PubPeer comments:
 Figure 3F and 3G appear to have images which overlap. *** ![file] *** ![file] , 
 Figures 4G and 4H appear to have images which overlap. These type of errors are sometimes seen in paper mill paper. *** ![file] , 
 Figure 7E and 7F appear to have images which overlap. *** ![file] ,
Energy Regulation Mechanism and Therapeutic Potential of Asprosin
Authors: Wei Xie
Jennifer G Hoffmann
Atul R Chopra
Journal: Diabetes (2020)
Discipline: CLINICAL MEDICINE
Keywords: neonatal progeroid syndrome; asprosin; profibrillin; OR4M1; glucogenic effect
Affiliations: Harrington Discovery Institute at University Hospitals, Cleveland, OH., Harrington Discovery Institute at University Hospitals, Cleveland, OH ., Department of Medicine, Case Western Reserve University, Cleveland, OH., Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH.

Abstract:  Genetic studies of patients with neonatal progeroid syndrome led to the discovery of the novel fasting-induced, glucogenic, and orexigenic hormone named asprosin, the C-terminal cleavage product of profibrillin. Upon secretion, asprosin travels to the liver, where it exerts a glucogenic effect through OR4M1, an olfactory G-protein-coupled receptor. It also crosses the blood-brain barrier to stimulate appetite-modulating neurons in the arcuate nucleus of the hypothalamus, exerting an orexigenic effect via an as yet unidentified receptor. Specifically, it stimulates appetite by activating orexigenic AgRP neurons and inhibiting anorexigenic POMC neurons. Studies have also focused on the therapeutic potential of inhibiting asprosin for treatment of obesity and type 2 diabetes, both of which are characterized by high levels of circulating asprosin. It has been shown that anti-asprosin monoclonal antibodies reduce blood glucose, appetite, and body weight, validating asprosin as a therapeutic target. Current work aims to uncover key features of the asprosin biology such as the identification of its neuronal receptor, identification of the secretion mechanism from adipose tissue, and development of anti-asprosin monoclonal antibodies as diabetes and obesity therapies. 

Retracted: No

PubPeer comments:
 But purified Asprosin has been shown to be ineffective by others: https: pubmed.ncbi.nlm.nih.gov 30879984 , 
 #1 But, effective by others: https: pubmed.ncbi.nlm.nih.gov 31230984 https: pubmed.ncbi.nlm.nih.gov 31798959 https: pubmed.ncbi.nlm.nih.gov 32337066 https: pubmed.ncbi.nlm.nih.gov 32329225 https: pubmed.ncbi.nlm.nih.gov 31230984 states  Of note, quality of asprosin protein is critical for its activity . Thus, seems like https: pubmed.ncbi.nlm.nih.gov 30879984 made poor quality asprosin protein and then found that it did not have activity. ,
Novel long noncoding RNA LINC01385 promotes nasopharyngeal carcinoma proliferation via the miR-140-3p/Twist1 signaling pathway
Authors: Lu Li
Feng Zhang
Journal: Cell Cycle (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Nasopharyngeal carcinoma; linc01385; miR-140-3p; twist1.
Affiliations: Department of Otology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, Henan, China.

Abstract:  Long non-coding RNAs (lncRNAs) have been verified as a key modulator in tumor progression. However, the functions of lncRNAs in nasopharyngeal carcinoma (NPC) remain unclear. In the present study, we explored lncRNAs expression patterns in NPC tissues by GEO dataset and selected the high expression lncRNA (LINC01385) to further study. Our data showed that LINC01385 expression was significantly increased NPC and correlated with advanced clinical features and poor prognosis. Function assays showed that knockdown of LINC01385 expression reduced the proliferation and invasion abilities of NPC cells in vitro. In mechanism, LINC01385 acted as a molecular sponge of miR-140-3p in NPC cells, Twist1 mRNA was validated as a direct target of miR-140-3p in NPC cells. The effects of the LINC01385 knockdown on malignant characteristics of NPC cells were greatly attenuated by miR-140-3p inhibition or Twist1 overexpression. Thus, we illustrated that LINC01385 aggravated the progression of NPC by sponging miR-140-3p and upregulating Twist1 expression, which implied LINC01385 might serve as a new potential therapeutic target for NPC treatment. 

Retracted: No

PubPeer comments:
 The paper reportedly used cement that was chemically and physically identical to that previously used by the group of Alireza Najigivi (see image below). This claim seems highly implausible, since the Najigivi group was working in Malaysia and the Nazari group was working in Iran. In a corrigendum by the Nazari group in a related work, it was stated that the work was originally performed by the Najigivi group. The source was not appropriately cited. ![file] , 
 Regarding ZnO2, please see the following thread: https: pubpeer.com publications 50205FFF072F536B7A4F8FBE5643C8 , 
 According to the respective Retraction Notes, material from this paper is duplicated in at least two now-retracted papers: -  Application of artificial neural networks for analytical modeling of Charpy impact energy of functionally graded steels (Nazari 2013) - Retracted [17 August 2020] . -  Prediction microhardness profile of functionally graded steels by ANFIS (Bohlooli et al 2013) - Retracted [25 August 2020] . Background here: https: retractionwatch.com 2019 10 15 a-researcher-with-30-retractions-and-counting-the-whistleblower-speaks ,
Mild and Chemoselective Thioacylation of Amines Enabled by the Nucleophilic Activation of Elemental Sulfur
Authors: Takeshi Nanjo
Sho Murakami
Masato Saito
Yoshiji Takemoto
Yusuke Kobayashi
Journal: Journal of the American Chemical Society (2020)
Discipline: CHEMISTRY
Keywords: thioacylation; amines; α-keto acids; elemental sulfur; nucleophilic activation
Affiliations: Graduate School of Pharmaceutical Sciences, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan.

Abstract:  A mild and chemoselective method for the thioacylation of amines using α-keto acids and elemental sulfur has been developed. The key to the success of this transformation is the nucleophilic activation of elemental sulfur by thiols such as 1-dodecanethiol. A variety of functional groups, including unprotected hydroxyl, carboxyl, amide, sulfide, and tertiary amine moieties, are tolerated under the applied reaction conditions. To demonstrate the advantages of this method compared with conventional O-S exchange reactions using Lawesson's reagent or P2S5, thioamide moieties were introduced site-specifically into biologically active compounds. 

Retracted: No

PubPeer comments:
 The reaction described in this paper is almost the same as that reported previously 86099-3). However, these reports are not referred to at all. If these previous reports were cited appropriately, the reviewers and editor of JACS should have doubted the novelty of this Takemoto s paper. ,
LncRNA DCRF regulates cardiomyocyte autophagy by targeting miR-551b-5p in diabetic cardiomyopathy
Authors: Weiting Xu
Wenjing Wang
Yu Feng
Wei Zhang
Xiang Zhou
Tong Liu
Journal: Theranostics (2019)
Discipline: CLINICAL MEDICINE
Keywords: DCRF; autophagy; diabetic cardiomyopathy; miR-551b-5p.
Affiliations: Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, China., Jiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University, Suzhou, China., Department of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Abstract:  Background: We generated a rat model of diabetic cardiomyopathy (DCM) and reported significant upregulation of the long non-coding RNA DCRF. This study was designed to determine the molecular mechanisms of DCRF in the development of DCM. Methods: Real-time PCR and RNA fluorescent in situ hybridization were conducted to detect the expression pattern of DCRF in cardiomyocytes. Histological and echocardiographic analyses were used to assess the effect of DCRF knockdown on cardiac structure and function in diabetic rats. mRFP-GFP-LC3 fluorescence microscopy, transmission electron microscopy, and Western blotting were carried out to determine cardiomyocyte autophagy. RNA immunoprecipitation and luciferase reporter assays were performed to elucidate the regulatory role of DCRF/miR-551b-5p/PCDH17 pathway in cardiomyocyte autophagy. Results: Our findings showed that DCRF knockdown reduced cardiomyocyte autophagy, attenuated myocardial fibrosis, and improved cardiac function in diabetic rats. High glucose increased DCRF expression and induced autophagy in cardiomyocytes. RNA immunoprecipitation and luciferase reporter assays indicated that DCRF was targeted by miR-551b-5p in an AGO2-dependent manner and PCDH17 was the direct target of miR-551b-5p. Forced expression of DCRF was found to attenuate the inhibitory effect of miR-551b-5p on PCDH17. Furthermore, DCRF knockdown decreased PCDH17 expression and suppressed autophagy in cardiomyocytes treated with high glucose. Conclusion: Our study suggests that DCRF can act as a competing endogenous RNA to increase PCDH17 expression by sponging miR-551b-5p, thus contributing to increased cardiomyocyte autophagy in DCM. 

Retracted: No

PubPeer comments:
 Two images in figure 2B appear to overlap. *** ![file] ,
Host cell poly(ADP-ribose) glycohydrolase is crucial for Trypanosoma cruzi infection cycle
Authors: Salomé C Vilchez Larrea
Silvia H Fernández Villamil
Mariana Schlesinger
Mirtha M Flawiá
María L Kevorkian
Guillermo D Alonso
Journal: PLoS ONE (2013)
Discipline: Multidisciplinary
Keywords: Trypanosoma cruzi; Chagas' disease; poly(ADP-ribose) glycohydrolase; TcPARG; gene conservation
Affiliations: Instituto de Investigaciones en Ingeniería Genética y Biología Molecular Dr. Héctor N. Torres, Consejo Nacional de Investigaciones Científicas y Técnicas, Ciudad Autónoma de Buenos Aires, Argentina.

Abstract:  Trypanosoma cruzi, etiological agent of Chagas' disease, has a complex life cycle which involves the invasion of mammalian host cells, differentiation and intracellular replication. Here we report the first insights into the biological role of a poly(ADP-ribose) glycohydrolase in a trypanosomatid (TcPARG). In silico analysis of the TcPARG gene pointed out the conservation of key residues involved in the catalytic process and, by Western blot, we demonstrated that it is expressed in a life stage-dependant manner. Indirect immunofluorescence assays and electron microscopy using an anti-TcPARG antibody showed that this enzyme is localized in the nucleus independently of the presence of DNA damage or cell cycle stage. The addition of poly(ADP-ribose) glycohydrolase inhibitors ADP-HPD (adenosine diphosphate (hydroxymethyl) pyrrolidinediol) or DEA (6,9-diamino-2-ethoxyacridine lactate monohydrate) to the culture media, both at a 1 µM concentration, reduced in vitro epimastigote growth by 35% and 37% respectively, when compared to control cultures. We also showed that ADP-HPD 1 µM can lead to an alteration in the progression of the cell cycle in hydroxyurea synchronized cultures of T. cruzi epimastigotes. Outstandingly, here we demonstrate that the lack of poly(ADP-ribose) glycohydrolase activity in Vero and A549 host cells, achieved by chemical inhibition or iRNA, produces the reduction of the percentage of infected cells as well as the number of amastigotes per cell and trypomastigotes released, leading to a nearly complete abrogation of the infection process. We conclude that both, T. cruzi and the host, poly(ADP-ribose) glycohydrolase activities are important players in the life cycle of Trypanosoma cruzi, emerging as a promising therapeutic target for the treatment of Chagas' disease. 

Retracted: No

PubPeer comments:
 Concern about Figure 4, shared with the journal in October 2015. Parts of the photos shown in the left panels (Figure 4A) appear to also be visible in the right panels (Figure 4B). Highlighted with red and blue boxes and arrows. ![file] , 
 #1 There are also a couple of other examples in the same panels, illustrated less elegantly below (using image with levels adjusted): ![file] ,
Nrf2 knockdown by shRNA inhibits tumor growth and increases efficacy of chemotherapy in cervical cancer
Authors: Detang Wang
Yanhong Huang
Shujuan Liu
Xiangdong Ma
Biliang Chen
Jianfang Zhang
Journal: Cancer Chemotherapy and Pharmacology (2012)
Discipline: CLINICAL MEDICINE
Keywords: Nrf2; cervical cancer; chemoresistance; antioxidant defense system; shRNA
Affiliations: Department of Obstetrics and Gynecology, Xijing Hospital, Fourth Military Medical University, 17 Changle West Road, Xi'an 710032, People's Republic of China.

Abstract:  Purpose: NF-E2-related factor 2 (Nrf2) is a key transcription regulator for cellular response to oxidative stress in normal cells. In cancer cells, development of chemoresistance is associated with the constitutive activation of the Nrf2-mediated antioxidant defense system. Here, we investigated the role of Nrf2 in terms of cervical cancer cell proliferation and drug resistance. Method: To investigate whether cancer cells activate the Nrf2 system, we examined 40 surgical cervical cancer samples and 12 normal control tissues. Plasmids containing Nrf2-small hairpin RNA (shRNA) or non-targeting vector-control shRNA were transfected into CaSki cells. Using Western blots and RT-PCR assays, the expression levels of Nrf2 mediated-target genes were measured in CaSki cells stably expressing Nrf2-shRNA. To evaluate how the Nrf2 knockdown affected susceptibility to chemotherapeutic drugs, MTT and flow cytometry assays were done in vitro and confirmed by a mouse xenograft model in vivo. Results: The Nrf2-dependent defensive system was likely fully activated in cervical tumor tissues. Genetic knockdown of endogenous Nrf2 caused a global decrease in expression of Nrf2-regulated genes. This decrease in expression levels enhanced chemotherapeutic drug-induced apoptotic death in CaSki cells with a reduced cellular glutathione level. Additionally, the combination of cisplatin treatment and Nrf2 knockdown significantly suppressed tumor growth in vivo. Conclusion: Our findings provide evidence that the inhibition of Nrf2 activity by shRNA might be a promising therapeutic strategy to enhance the efficacy of anticancer drugs and thus can be applied further during the course of chemotherapy in the treatment of cervical cancer. 

Retracted: No

PubPeer comments:
 Concern about Figure 4. The flow cytometry panels all show different experiments, but appear to show elements visible in multiple panels, or multiple times within the same panel. Shown with colored rounded rectangles.  This research was supported by the National Science Foundation of China (NSFC 50577067). The funding sources had input into the design of this study, the collection, analysis and interpretation of data. This concern was shared with the journal 4 years ago, but this issue remains unaddressed as of today. The journal still charges $40 for access. ![file] , 
 An updated version of Figure 4. ![file] ,
LncRNA DANCR promotes migration and invasion through suppression of lncRNA-LET in gastric cancer cells
Authors: Xiangyu Zhao
Yuguang Xing
Zhengqiang Mao
Hang Li
Botao Du
Kai Cui
Shoufeng Zai
Journal: Bioscience reports (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: DANCR; EZH2; HDAC3; lncRNA-LET.
Affiliations: Department of Surgical Oncology, Xinxiang Central Hospital, Xinxiang, Henan Province, China., Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China., Department of Surgical Oncology, Xinxiang Central Hospital, Xinxiang, Henan Province, China .

Abstract:  Gastric cancer (GC) is one of the most prevalent gastrointestinal malignancies. Long noncoding RNA (lncRNA) DANCR is a newly identified oncogenic lncRNA. However, the functional role and underlying molecular mechanisms of DANCR involved in GC progress remain unclear. In the present study, we investigated the biological function and underlying mechanisms of DANCR in GC cell migration and invasion. The results showed that knockdown of DANCR inhibited migration and invasion of GC cells, whereas overexpression of DANCR showed the opposite effect. Further investigation demonstrated that lncRNA-LET was a bona fide target gene of DANCR. In addition, high DANCR and low lncRNA-LET were significantly correlated with lymph node metastasis and late clinical stage. DANCR associated with EZH2 and HDAC3 to epigenetically silence lncRNA-LET and then regulated GC migration and invasion. Taken together, these findings indicate an important role for DANCR-lncRNA-LET axis in GC cell migration and invasion, and reveal a novel epigenetic mechanism for lncRNA-LET silencing. 

Retracted: No

PubPeer comments:
 Fig 1.  TEM of Amp B nano-suspension . ![file] Figure 1(a) from [Khurana et al (2013)] .  TEM photomicrograph of developed nanocarriers: (a) chitosan nanoparticles . ![file] They seem to be the same image. ,
Retracted Article: Enhanced adsorption of ionizable aromatic compounds on humic acid-coated carbonaceous adsorbents
Authors: Yubing Sun
Changlun Chen
Dadong Shao
Jiaxing Li
Xiaoli Tan
Guixia Zhao
Shubin Yang
Xiangke Wang
Journal: RSC Advances (2012)
Discipline: CHEMISTRY
Keywords: Adsorption; Ionizable aromatic compounds; Humic acid; Graphene oxide nanosheets; Multiwalled carbon nanotubes
Affiliations: Key Laboratory of Novel Thin Film Solar Cells, Institute of Plasma Physics, Chinese Academy of Sciences, Hefei 230031, P. R. China

Abstract: Adsorption of ionizable aromatic compounds (IACs) such as 1-naphthylamine and 1-naphthol on Humic acid (HA)-coated graphene oxide nanosheets (GONs), multiwalled carbon nanotubes (MWCNTs), activated carbon (AC), and flake graphite (FG) were investigated by the batch techniques. The adsorption of 1-naphthylamine on four HA-coated carbonaceous adsorbents was weakly depended on pH, whereas the adsorption of 1-naphthol on these HA-coated carbonaceous adsorbents evidently increased with increasing pH from 2.0 to 8.0. The maximum adsorption capacity of HA-coated carbonaceous adsorbents for IACs was in the order of GONs\u226bMWCNTs>AC>FG, indicating that the GONs can be regarded as a suitable material for the preconcentration and removal of IACs from aqueous solution in environmental pollution management. The main adsorption mechanism between carbonaceous adsorbents and IACs is the hydrophobic effect. This observation is of great implication for the removal of IACs by HA-coated carbonaceous adsorbents in environmental applications.

Retracted: Yes

PubPeer comments:
 Figure 1. Much more similar than expected. https: imgur.com 7PWu76w , 
 #1 Figure 1 continued. Much more similar than expected. https: imgur.com OI3HB4o ,
Arsenic trioxide regulates gastric cancer cell apoptosis by mediating cAMP
Authors: A Abudoureyimu
A Muhemaitibake
Journal: European Review for Medical and Pharmacological Sciences (2017)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Gastric cancer; arsenic trioxide; apoptosis; BGC-823 cells; cAMP
Affiliations: Department of Geriatrics, Xinjiang Medical University Affiliated Hospital of Traditional Chinese Medicine, Urumqi, Xinjiang, China. .

Abstract:  Objective: Gastric cancer is a common digestive tract tumor in clinic with increasing incidence. It is suggested that arsenic trioxide (As2O3) has an inhibitory effect on many kinds of digestive system tumors. This study evaluated the impact of As2O3 on the apoptosis of gastric cancer BGC-823 cells, and analyzed its relationship with cyclic adenosine monophosphate (cAMP). Materials and methods: Gastric cancer cell BGC-823 was intervened by different concentrations of As2O3 at 4 ng/ml, 8 ng/ml, and 16 ng/ml, respectively. BGC-823 cell apoptosis was evaluated by TUNEL assay. Cell cycle was determined by flow cytometry. cAMP and protein kinase C (PKC) was detected by radioimmunoassay. Apoptosis-related protein levels were tested by Western blot. Results: Compared with normal control, As2O3 significantly increased BGC-823 cell apoptosis, blocked cell cycle in G0/G1 phase, elevated cAMP and Bax level, as well as downregulated PKC, Bcl-2 and Survivin expression (p &lt; 0.05). Conclusions: As2O3 induced BGC-823 cell apoptosis through the up-regulation of the cAMP level and the decrease of the PKC level. 

Retracted: No

PubPeer comments:
 Figure 2 in this paper appears to show some overlapping panels, as well as overlaps with Figure 1 of XM Liu et al. 2017, ERMPS, PubMed ID: 28682425. Areas that look similar are highlighted with boxes of the same color. Of additional concern are similarities between this Figure 1 (see comment #1) and Figure 2 in A Abudoureyimu and A Muhemaitibake, 2017, ERMPS, Pubmed ID: 28239804 . It is not clear what Figure 1 in the other paper is showing (the experimental conditions did not differ in the concentration of something, but rather had different ischemia and reperfusion times). Figure 2 in this paper shows BGC-823 cells treated with Arsenic trioxide. Could the authors please clarify which experiments we are looking at here? ![file] ,
Inhibition of CD147 gene expression via RNA interference reduces tumor cell proliferation, activation, adhesion, and migration activity in the human Jurkat T-lymphoma cell line
Authors: Fang Yang
Jing Chang
Juan Su
Jiang Lin Zhang
Ji Li
Hui Lu
Takuro Kanekura
Xiang Chen
Ye Hong Kuang
Sheng Peng
Journal: Cancer Investigation (2008)
Discipline: CLINICAL MEDICINE
Keywords: CD147; T-lymphoma; leukocyte; proteinase production; fibroblasts
Affiliations: Department of Dermatology, XiangYa Hospital, Central South University, Changsha, Hunan, China. 

Abstract:  CD147, a leukocyte surface molecule over-expressed in T-lymphoma cells, is reportedly associated with lymphocyte activation and proteinase production via interactions with fibroblasts and plays a role in stromal invasion by lymphoma cells. To determine the role of CD147 in the progression of T-lymphoma, we performed siRNA interference-mediated knockdown of CD147 in a CD147-expressing Jurkat T-cell line. CD147 knockdown resulted in the decreased proliferation and migration of Jurkat cells and reduced the adhesion of Jurkat cells to extracelluar matrix fibronectin in vitro. CD147-siRNA inhibited the activation of Jurkat cells via down-regulation of CD25 expression. Our results indicate that CD147 is involved in T-lymphoma progression, a finding useful in efforts to develop targeted therapies to treat patients with T-lymphoma. 

Retracted: No

PubPeer comments:
 Concern about Figure 4B, reported to the journal in 2015. Some cells or groups of cells appear to be visible multiple times across panels. Circles of the same color highlight those similar-looking cells. ![file] ,
The dependence receptor UNC5H2/B triggers apoptosis via PP2A-mediated dephosphorylation of DAP kinase
Authors: Galit Shohat
Céline Guenebeaud
Patrick Mehlen
Guillaume Chazot
Adi Kimchi
Vincent Laudet
David Goldschneider
Marie Castets
Avital Eisenberg-Lerner
Céline Delloye-Bourgeois
Mingjie Zhang
Agnès Bernet
Catherine Guix
Journal: Molecular Cell (2010)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: UNC5H dependence receptors; apoptosis; netrin-1; neuronal development; vascular development
Affiliations: Apoptosis, Cancer and Development Laboratory-Equipe Labellisée "La Ligue," CNRS UMR5238, Université de Lyon, Centre Léon Bérard, 69008 Lyon, France.

Abstract:  The UNC5H dependence receptors promote apoptosis in the absence of their ligand, netrin-1, and this is important for neuronal and vascular development and for limitation of cancer progression. UNC5H2 (also called UNC5B) triggers cell death through the activation of the serine-threonine protein kinase DAPk. While performing a siRNA screen to identify genes implicated in UNC5H-induced apoptosis, we identified the structural subunit PR65β of the holoenzyme protein phosphatase 2A (PP2A). We show that UNC5H2/B recruits a protein complex that includes PR65β and DAPk and retains PP2A activity. PP2A activity is required for UNC5H2/B-induced apoptosis, since it activates DAPk by triggering its dephosphorylation. Moreover, netrin-1 binding to UNC5H2/B prevents this effect through interaction of the PP2A inhibitor CIP2A to UNC5H2/B. Thus we show here that, in the absence of netrin-1, recruitment of PP2A to UNC5H2/B allows the activation of DAPk via a PP2A-mediated dephosphorylation and that this mechanism is involved in angiogenesis regulation. 

Retracted: No

PubPeer comments:
null, 
null, 
null, 
null, 
null, 
null, 
 #4 This issue does not appear to have been addressed. Figure retrieved today shows below. *** ![file] ,
A new porous cationic metal–organic framework: selective sorption of organic dyes and treatment on neural stem cells during spinal cord injury treatment
Authors: Cao, Cong
Li, Zhi-Zhang
Zhang, Zai-Qing
Chen, Xuan-Huang
Journal: Journal of the Iranian Chemical Society (2020)
Discipline: CHEMISTRY
Keywords: metal-organic framework; Co(II); methylene blue; nerve growth factor; spinal cord injury

Abstract: A novel metal–organic framework containing Co(II) of {(Me2NH2)4[Co12(OH)4(abtc)6 (H2O)12]·14H2O}n (1) has been synthesized via Co(NO3)2·6H2O to react with the 3,3′,5,5′-azobenzenetetracarboxylic acid (H4abtc) ligand under solvothermal conditions. Furthermore, methylene blue (MB) can easily replace free cations; after half a day, more than 90% of the MB (10\u22125 M) is absorbed selectively, and it makes the title compound become a good medium for the separation and adsorption of the dye. In biological section, the enhancement activity of the compound on the nerve growth factor for the spinal cord injury treatment was evaluated. The relative gene expression of trkA receptor was measured with reverse transcription polymerase chain reaction. In addition to this, the activation of PI3K/Akt signaling pathway in neural stem cells after treated by compound was evaluated with western blot. The results of potential binding models were predicted by molecular docking, and the binding poses provided possible binding mechanisms of the functional groups of the complex to the TRKA protein.

Retracted: No

PubPeer comments:
  The results show that the ligands involving nitrogen atoms and polycarboxylate have multiple binding nodes, which can be widely utilized in the construction of MOFs [15u201319]. - [16]. W. Liu, H. Li, H. Zhu, P. Xu, Materials 13, 1180 (2020) ** The Interfacial Adhesion Performance and Mechanism of a Modified Asphaltu2013Steel Slag Aggregate ** Really? Fig 2  b The curve of TGA for the complex 1 ![file] *[left]* Fig 2b from [Hou et al (2020)] . *[right]* Fig 2b from [Ma et al (2020)] . Many other manifestations are linked in those threads ![file] Surprisingly similar TGA curves, from two different materials. Here superimposed: ![file] ,
Efficient Fluoride Removal from Aqueous Solution Using Zirconium-Based Composite Nanofiber Membranes
Authors: Tawheed Hashem
Ammar Mahmood
Evgenia Bogdanova
Elvia P Valadez Sanchez
Alaa Mohamed
Roman V Ostvald
Britta Bergfeldt
Journal: Membranes (2021)
Discipline: CHEMISTRY
Keywords: UiO-66; UiO-66-NH2; adsorption mechanisms; metal-organic framework; water treatment.
Affiliations: Institute of Functional Interfaces (IFG), Karlsruhe Institute of Technology (KIT), Hermann-von Helmholtz-Platz 1, 76344 Eggenstein-Leopoldshafen, Germany., School of Nuclear Science and Engineering, National Research Tomsk Polytechnic University, 634050 Tomsk, Russia., Institute for Technical Chemistry (ITC), Karlsruhe Institute for Technology (KIT), Hermann-von Helmholtz-Platz 1, 76344 Eggenstein-Leopoldshafen, Germany.

Abstract:  Herein, composite nanofiber membranes (CNMs) derived from UiO-66 and UiO-66-NH2 Zr-metal-organic frameworks (MOFs) were successfully prepared, and they exhibited high performance in adsorptive fluoride removal from aqueous media. The resultant CNMs were confirmed using different techniques, such as X-ray diffraction (XRD), field emission scanning electron microscopy (FE-SEM), and Brunauer-Emmett-Teller (BET) in addition to Fourier-transform infrared spectroscopy (FTIR). The parameters that govern the fluoride adsorption were evaluated, including adsorbent dose, contact time, and pH value, in addition to initial concentration. The crystalline structures of CNMs exhibited high hydrothermal stability and remained intact after fluoride adsorption. It could also be observed that the adsorbent dose has a significant effect on fluoride removal at high alkaline values. The results show that UiO-66-NH2 CNM exhibited high fluoride removal due to electrostatic interactions that strongly existed between F- and metal sites in MOF in addition to hydrogen bonds formed with MOF amino groups. The fluoride removal efficiency reached 95% under optimal conditions of 20 mg L-1, pH of 8, and 40% adsorbent dose at 60 min. The results revealed that UiO-66-NH2 CNM possesses a high maximum adsorption capacity (95 mg L-1) over UiO-66 CNM (75 mg L-1), which exhibited better fitting with the pseudo-second-order model. Moreover, when the initial fluoride concentration increased from 20 to 100 mg/L, fluoride adsorption decreased by 57% (UiO-66 CNM) and 30% (UiO-66-NH2 CNM) after 60 min. After three cycles, CNM revealed the regeneration ability, demonstrating that UiO-66-NH2 CNMs are auspicious adsorbents for fluoride from an aqueous medium. 

Retracted: No

PubPeer comments:
 Pointed out to me by a reader: * Green boxes: part of the SEM image in Figure 1E (CNM after adsorption) appears to show the same nanofibers as the SEM image in Figure 6B (CNM after various cycles of recycling. ![file] ,
Ataxin-2 interacts with FUS and intermediate-length polyglutamine expansions enhance FUS-related pathology in amyotrophic lateral sclerosis
Authors: Ian P Blair
Julie D Atkin
Manal A Farg
Vinod Sundaramoorthy
Sadaf T Warraich
Kai Y Soo
Journal: Human Molecular Genetics (2013)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Fused in sarcoma; FUS; amyotrophic lateral sclerosis; ALS; neurodegeneration
Affiliations: Department of Biochemistry, La Trobe University, Vic., Australia.

Abstract:  Fused in sarcoma (FUS) is mutated in both sporadic amyotrophic lateral sclerosis (ALS) and familial ALS patients. The mechanisms underlying neurodegeneration are not fully understood, but FUS redistributes from the nucleus to the cytoplasm in affected motor neurons, where it triggers endoplasmic reticulum (ER) stress. Ataxin-2 is a polyglutamine protein which normally contains 22 repeats, but expanded repeats (&gt;34) are found in Spinocerebellar Ataxia type 2. Recently ataxin-2 with intermediate length repeats (27-33) was found to increase the risk of ALS. Here we show that ataxin-2 with an ALS-linked intermediate length repeat (Q31) is a potent modifier of FUS pathology in cellular disease models. Translocation of FUS to the cytoplasm and ER stress were significantly enhanced by co-expression of mutant FUS with ataxin-2 Q31. Ataxin-2 also co-localized with FUS in sporadic and FUS-linked familial ALS patient motor neurons, co-precipitated with FUS in ALS spinal cord lysates, and co-localized with FUS in the ER-Golgi compartments in neuronal cell lines. Fragmentation of the Golgi apparatus is linked to neurodegeneration in ALS and here we show that Golgi fragmentation is induced in cells expressing mutant FUS. Moreover, Golgi fragmentation was enhanced, and the early stages of apoptosis were triggered, when ataxin-2 Q31 was co-expressed with mutant FUS. These findings describe new cellular mechanisms linking ALS with ataxin-2 intermediate length polyQ expansions and provide further evidence linking disruption to ER-Golgi compartments and FUS pathology in ALS. 

Retracted: No

PubPeer comments:
 In Figure 2C, the FUS bands look unexpectedly similar to the beta-actin bands![file] , 
 Correction published to Fig. 2: Hum Mol Genet. 2020 Mar 13;29(4):703-704. doi: 10.1093 hmg ddz313. In the correction, it is unclear what  N refers to, and in part C, why the same blot shows both FUS and actin, even though it was stripped. ![file] ,
Ruscogenin induces ferroptosis in pancreatic cancer cells
Authors: Ziling Fang
Jianping Xiong
Xiaojun Xiang
Junhe Li
Zhiwang Song
Ling Zhang
Jun Deng
Journal: Oncology Reports (2019)
Discipline: CLINICAL MEDICINE
Keywords: ruscogenin; pancreatic cancer; ferroptosis; anticancer.
Affiliations: Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

Abstract:  Pancreatic cancer is characterized by aggressive and highly metastatic phenotypes. This disease exhibits a poor patient prognosis and is considered a challenge due to the limited treatment options encountered in clinical practice. Previous studies have shown that ruscogenin, a saponin found in the root of Ophiopogon japonicus, exerts a wide range of biological functions including anticancer activity. In the present study, the effects of ruscogenin were investigated on pancreatic cancer cells and the potential molecular mechanism of this compound was explored. Cell viability was assessed using the 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide (MTT) assay. Cell death was measured by trypan blue staining and by flow cytometry. The number of iron oxide nanoparticles was measured using Prussian blue staining. Reactive oxygen species (ROS) production was assessed using flow cytometry with dihydroethidium staining. Protein expression of the associated genes was assayed by western blotting. Furthermore, in vivo experiments were conducted to confirm the antitumor effects and assay the potential toxicity of ruscogenin in a nude mouse xenograft model. The results indicated that ruscogenin significantly repressed cell viability and induced cell death of pancreatic cancer cells in vitro in a dose‑ and time‑dependent manner. Furthermore, ruscogenin increased the concentration of intracellular ferrous irons and the production of ROS. This effect was inhibited by deferoxamine (DFO). Ruscogenin induced ferroptosis by regulating the levels of transferrin and ferroportin. These two proteins were involved in ruscogenin‑induced pancreatic cancer cell death. Finally, in vivo experiments demonstrated the antitumor effect of ruscogenin on pancreatic cancer xenografts in the absence of apparent toxicity. Taken collectively, the data demonstrated that ruscogenin exhibited anticancer effects in pancreatic cancer cells by inducing ferroptosis. The findings suggested that this compound may be further developed as a promising anticancer candidate for the treatment of pancreatic cancer. 

Retracted: No

PubPeer comments:
 ![Song_2020_fig_7a] This is figure 7a In the second row the shadow of the rightmost tumor appears to be rotated 90u00b0 counter clockwise ,
FSD-C10, a Fasudil derivative, promotes neuroregeneration through indirect and direct mechanisms
Authors: Guang-Xian Zhang
Rodolfo Thome
Qing Wang
Cun-Gen Ma
Hai-Fei Zhang
Xing Li
Zhi Chai
Yan-Hua Li
Yuan Zhang
Bao-Guo Xiao
Chong Xie
Journal: Scientific reports (2017)
Discipline: Multidisciplinary
Keywords: FSD-C10; experimental autoimmune encephalomyelitis; multiple sclerosis; immune response; neuroprotective molecules
Affiliations: Institute of Brain Science, Datong key Laboratory of Molecular and Cell Immunology, Shanxi Datong University, Datong, 037009, China., Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA., "2011" Collaborative Innovation Center/Research Center of Neurobiology, Shanxi University of Traditional Chinese Medicine, Taiyuan 030024, China., Institute of Neurology, Huashan Hospital, Institutes of Brain Science and State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, 200025, China.

Abstract:  FSD-C10, a Fasudil derivative, was shown to reduce severity of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), through the modulation of the immune response and induction of neuroprotective molecules in the central nervous system (CNS). However, whether FSD-C10 can promote neuroregeneration remains unknown. In this study, we further analyzed the effect of FSD-C10 on neuroprotection and remyelination. FSD-C10-treated mice showed a longer, thicker and more intense MAP2 and synaptophysin positive signal in the CNS, with significantly fewer CD4+ T cells, macrophages and microglia. Importantly, the CNS of FSD-C10-treated mice showed a shift of activated macrophages/microglia from the type 1 to type 2 status, elevated numbers of oligodendrocyte precursor cells (OPCs) and oligodendrocytes, and increased levels of neurotrophic factors NT-3, GDNF and BDNF. FSD-C10-treated microglia significantly inhibited Th1/Th17 cell differentiation and increased the number of IL-10+ CD4+ T cells, and the conditioned medium from FSD-C10-treated microglia promoted OPC survival and oligodendrocyte maturation. Addition of FSD-C10 directly promoted remyelination in a chemical-induced demyelination model on organotypic slice culture, in a BDNF-dependent manner. Together, these findings demonstrate that FSD-C10 promotes neural repair through mechanisms that involved both immunomodulation and induction of neurotrophic factors. 

Retracted: No

PubPeer comments:
 Figure 3c, 4c, and 5a use the same beta-actin bands : ![file] ,
Knockdown of lncRNA XIST inhibits retinoblastoma progression by modulating the miR-124/STAT3 axis
Authors: Chunling Xu
Mei Han
Yingxue Wang
Shu Liu
Chunmei Hu
Journal: Biomedicine & Pharmacotherapy (2018)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: LncRNA; Retinoblastoma; STAT3; XIST; miR-124.
Affiliations: Department of Tumor and Hematology, The Second Hospital of Jilin University, Nanguan District, Changchun, Jilin, 130041, PR China., Department of Ophthalmology, The Second Hospital of Jilin University, Nanguan District, Changchun, Jilin, 130041, PR China., Department of Electrical Diagnosis, The Second Hospital of Jilin University, Nanguan District, Changchun, Jilin, 130041, PR China., Department of Ophthalmology, The Second Hospital of Jilin University, Nanguan District, Changchun, Jilin, 130041, PR China. Electronic address: .

Abstract:  This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief and the authors. Figure 2D appears similar to Figure 2D of the article that Dongkai Zhao, Zhiyu Jiang, Zhihui Wang and Jinliang Gao have previously published in Biomedicine &amp; Pharmacotherapy 98 (2018) 719-725 https://doi.org/10.1016/j.biopha.2017.12.114. However, the images purport to represent different experiments by separate author groups. The authors offer their apologies to the readers of the journal for any inconvenience this might have caused. 

Retracted: Yes

PubPeer comments:
 Two papers used the same flow-cytometry histograms to support their claims to have conducted (different) experiments. No authors in common. How did this happen? *[left]* Fig 2F.  Flow cytometer detects cell arrest in SO-RB-50 cells transfected with si-NC or si-XIST. *[right]* Fig 2D from [Zhao et al (2018)] .  Cell cycle arrest was measured in RA-FLS after the transfection of pCDNA3.1-GRIM19 and pCDNA3.1. ![file] , 
 Retracted [11 March 2022] . ----------------------------- This article has been retracted at the request of the Editor-in-Chief and the authors. Figure 2D appears similar to Figure 2D of the article that Dongkai Zhao, Zhiyu Jiang, Zhihui Wang and Jinliang Gao have previously published in Biomedicine Pharmacotherapy 98 (2018) 719-725 https: doi.org 10.1016 j.biopha.2017.12.114. However, the images purport to represent different experiments by separate author groups. The authors offer their apologies to the readers of the journal for any inconvenience this might have caused. ,
Malignant bowel obstruction in advanced cancer patients: epidemiology, management, and factors influencing spontaneous resolution
Authors: Nuria Codorniu
Emilio Martinez-Losada
Albert Tuca
Ernest Guell
Journal: Cancer management and research (2012)
Discipline: CLINICAL MEDICINE
Keywords: bowel occlusion; cancer; intestinal obstruction; malignant bowel obstruction.
Affiliations: Cancer and Hematological Diseases Institute, Hospital Clínic de Barcelona, Barcelona, Spain.

Abstract:  Malignant bowel obstruction (MBO) is a frequent complication in advanced cancer patients, especially in those with abdominal tumors. Clinical management of MBO requires a specific and individualized approach that is based on disease prognosis and the objectives of care. The global prevalence of MBO is estimated to be 3% to 15% of cancer patients. Surgery should always be considered for patients in the initial stages of the disease with a preserved general status and a single level of occlusion. Less invasive approaches such as duodenal or colonic stenting should be considered when surgery is contraindicated in obstructions at the single level. The priority of care for inoperable and consolidated MBO is to control symptoms and promote the maximum level of comfort possible. The spontaneous resolution of an inoperable obstructive process is observed in more than one third of patients. The mean survival is of no longer than 4-5 weeks in patients with consolidated MBO. Polymodal medical treatment based on a combination of glucocorticoids, strong opioids, antiemetics, and antisecretory drugs achieves very high symptomatic control. This review focuses on the epidemiological aspects, diagnosis, surgical criteria, medical management, and factors influencing the spontaneous resolution of MBO in advanced cancer patients. 

Retracted: No

PubPeer comments:
 It seems that this article is plagiarised by another articleuff08Rao B, Shi H. Malignant bowel obstruction: a struggle of technology, emotion and hope. Electron J Metab Nutr Cancer. 2017; 4:136-143.uff09 The second paper is just copying and translating the first paper into a second language without adding any innovation. 1. Tuca A, Guell E, Martinez-Losada E, Codorniu N. Malignant bowel obstruction in advanced cancer patients: epidemiology, management, and factors influencing spontaneous resolution. Cancer Manag Res. 2012; 4:159-169. DOI: 10.2147 CMAR.S29297 Full text link: https: www.dovepress.com getfile.php?fileID=12955 2. Rao B, Shi H. Malignant bowel obstruction: a struggle of technology, emotion and hope. Electron J Metab Nutr Cancer. 2017; 4:136-143. (In Chinese) DOI: 10.16689 j.cnki.cn11-9349 r.2017.02.002 Full text link: http: www.ejmnc.org CN article downloadArticleFile.do?attachType=PDF id=177 The problems are highlighted with yellow, and are marked with red box and arrow. ![file] ![file] ![file] ![file] ![file] ![file] ,