PReD-Bench/PRed-Bench huggingface dataset:
Inhibition of Caspase 3 Abrogates Lipopolysaccharide-Induced Nitric Oxide Production by Preventing Activation of NF-κB and c-Jun NH 2 -Terminal Kinase/Stress-Activated Protein Kinase in RAW 264.7 Murine Macrophage Cells
Authors: M M Mu
N Koide
D Chakravortty
T Sugiyama
T Yoshida
Y Kato
T Yokochi
Journal: Infection and Immunity (2001)
Discipline: IMMUNOLOGY
Keywords: caspase inhibitors; lipopolysaccharide; nitric oxide production; RAW 267.4; murine macrophage cells
Affiliations: Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan., <!--label omitted: 1-->Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan

Abstract:  The effect of caspase inhibitors on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW 267.4 murine macrophage cells was investigated. Pretreatment of RAW cells with a broad caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK), resulted in a striking reduction in LPS-induced NO production. Z-VAD-FMK inhibited LPS-induced NF-kappaB activation. Furthermore, it blocked phosphorylation of c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) but not that of extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinases. Similarly, a caspase 3-specific inhibitor, Z-Asp-Glu-Val-Asp-fluoromethylketone, inhibited NO production, NF-kappaB activation, and JNK/SAPK phosphorylation in LPS-stimulated RAW cells. The attenuated NO production was due to inhibition of the expression of an inducible-type NO synthase (iNOS). The overexpression of the dominant negative mutant of JNK/SAPK and the addition of a JNK/SAPK inhibitor blocked iNOS expression but did not block LPS-induced caspase 3 activation. It was therefore suggested that the inhibition of caspase 3 might abrogate LPS-induced NO production by preventing the activation of NF-kappaB and JNK/SAPK. The caspase family, especially caspase 3, is likely to play an important role in the signal transduction for iNOS-mediated NO production in LPS-stimulated mouse macrophages. 

Retracted: No

PubPeer comments:
 Much more similar than expected ![file] , 
 ![file] ,
NF-κB suppresses apoptosis and promotes bladder cancer cell proliferation by upregulating survivin expression in vitro and in vivo
Authors: Chuize Kong
Dezhi Shen
Zhe Zhang
Yu Zeng
Xiankui Liu
Xuyong Lin
Xiaolu Cui
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: NF-κB activation; survivin; bladder cancer; YM-155; cell cycle progression
Affiliations: Department of Urology, The First Hospital of China Medical University, Shenyang 110001, Liaoning, China., Department of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang 110001, Liaoning, China.

Abstract:  Nuclear factor kappa-B (NF-κB) activation is a common phenomenon in cancers, which results in the aberrant expression of NF-κB target genes and leads to malignant transformation, metastatic dissemination, abnormal cell proliferation or resistance to cell death. Survivin is a unique member of the IAP family, a well-known cancer-specific molecule and a molecular marker of poor clinical outcome in several cancer types, including bladder cancer. YM-155, a potent survivin suppressor, has been shown to have anti-tumor activity in preclinical cell lines, xenograft models and phase I/II studies. In the present study, we investigated the function of the NF-κB/survivin pathway in bladder cancer. We found that NF-κB can promote cell cycle progression and reduce apoptosis by upregulating survivin expression, thereby increasing cellular proliferation. We further confirmed the tumorigenic function of the NF-κB/survivin pathway in vivo using a xenograft tumor model of stable NF-κB-overexpressing 5637 cells. Moreover, we found that YM-155 significantly induced apoptosis and decreased cellular proliferation as well as tumor growth in mice. Our results demonstrate the carcinogenic function of the NF-κB/survivin pathway in bladder cancer and the role of YM-155 as a promising agent for the strategic treatment of bladder cancer. 

Retracted: No

PubPeer comments:
 In Figure 6C, a micrograph has been duplicated and presented as something else (red squares). In addition, two micrographs have been duplicated and presented as something else between Figure 6C and 2A (black and orange squares). ![file] ,
Hydrogen Sulfide Recruits Macrophage Migration by Integrin β1-Src-FAK/Pyk2-Rac Pathway in Myocardial Infarction
Authors: Yi-Zhun Zhu
Hong Xin
Lei Miao
Xiaoming Xin
Xiaoyan Shen
Journal: Scientific Reports (2016)
Discipline: Multidisciplinary
Keywords: Myocardial infarction; macrophages; inflammation; tissue repairing; infiltration
Affiliations: Department of Pharmacology, School of Pharmacy and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.

Abstract:  Myocardial infarction (MI) triggers an inflammatory reaction, in which macrophages are of key importance for tissue repairing. Infiltration and/or migration of macrophages into the infarct area early after MI is critical for infarct healing, vascularization, and cardiac function. Hydrogen sulfide (H2S) has been demonstrated to possess cardioprotective effects post MI and during the progress of cardiac remodeling. However, the specific molecular and cellular mechanisms involved in macrophage recruitment by H2S remain to be identified. In this study, the NaHS (exogenous sources of H2S) treatment exerted an increased infiltration of macrophages into the infarcted myocardium at early stage of MI cardiac tissues in both wild type (WT) and cystathionine-γ-lyase-knockout (CSE-KO) mice. And NaHS accelerated the migration of macrophage cells in vitro. While, the inhibitors not only significantly diminished the migratory ability in response to NaHS, but also blocked the activation of phospho-Src, -Pyk2, -FAK(397), and -FAK(925). Furthermore, NaHS induced the internalization of integrin β1 on macrophage surface, but, integrin β1 silencing inhibited macrophage migration and Src signaling activation. These results indicate that H2S may have the potential as an anti-infarct of MI by governing macrophage migration, which was achieved by accelerating internalization of integrin β1 and activating downstream Src-FAK/Pyk2-Rac pathway. 

Retracted: No

PubPeer comments:
 Figure 1c. https: imgur.com Z88fF01 , 
 Figure 5c. https: imgur.com 9zmfnW9 ,
Long non-coding RNA TUG1 promotes migration and invasion by acting as a ceRNA of miR-335-5p in osteosarcoma cells
Authors: Weiguo Zhang
Wei Zhao
Yong Wang
Zhen Zhang
Xiandong Zeng
Tao Yang
Ming Lu
Journal: Cancer Science (2017)
Discipline: CLINICAL MEDICINE
Keywords: ceRNA; lncRNA TUG1; miR-335-5p; migration/invasion; osteosarcoma.
Affiliations: The 4th Department of Orthopedic Surgery, Central Hospital Affiliated to Shenyang Medical College, Shenyang, China., Department of Joint Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, China., Department of Surgery Oncology, Central Hospital Affiliated to Shenyang Medical College, Shenyang, China.

Abstract:  Long non-coding RNA (lncRNA) have been the focus of increasing attention due to the role they play in many diseases, including osteosarcoma. The function of taurine upregulated gene 1 (TUG1) and its mechanism in osteosarcoma remain unclear. In our research, we found that TUG1 was elevated and correlated with a poor prognosis in osteosarcoma patients. In addition, the following functional experiment showed that decreased TUG1 could remarkably inhibit osteosarcoma cell migration and invasion, indicating that TUG1 functioned as an oncogene in osteosarcoma. Moreover, we revealed that TUG1 and Rho-associated coiled-coil-containing protein kinase 1 (ROCK1), a metastasis-related gene targeted by microRNA-335-5p (miR-335-5p), had the same miR-335-5p combining site. The subsequent luciferase assay verified TUG1 was a target of miR-335-5p. Furthermore, the results of a real-time quantitative PCR showed that TUG1 and miR-335-5p could affect each other's expression. respectively. Finally, we affirmed that TUG1 affected ROCK1 expression and ROCK1-mediated migration/invasion by working as a competitive endogenous RNA (ceRNA) via miR-335-5p. In summary, the findings of this study, based on ceRNA theory, combining the research foundation of miR-335-5p and ROCK1, and taking TUG1 as a new study point, provide new insight into molecular-level reversing migration and invasion of osteosarcoma. 

Retracted: No

PubPeer comments:
  Osteosarcoma tissues and paired para-tumor bone tissues used in this study were collected from 44 patients, with their permission, during tumorectomy at the First Affiliated Hospital of Dalian Medical University Central Hospital affiliated to Shenyang Medical College between **February 2008 and February 2016**. According to Fig 1(c), patient survival was followed for 10 years after recruitment, i.e. through to the period **February 2018 to February 2026**. Fig 1(c),  Kaplanu2013Meier analyses of the associations between TUG1 expression level and overall survival of patients with osteosarcoma . ![file] How does this work, for a paper submitted on December 14, 2016? Was a time machine involved? ,
Stimuli-responsive materials prepared from carboxymethyl chitosan and poly(γ-glutamic acid) for protein delivery
Authors: Shu-Huei Yu
Yi-Cheng Ho
Shao-Jung Wu
Fwu-Long Mi
Hsing-Wen Sung
Deh-Wei Tang
Tzu-Hung Kuo
Journal: Carbohydrate Polymers (2012)
Discipline: CHEMISTRY
Keywords: Chitosan; Genipin; Protein delivery; Stimuli-responsive.
Affiliations: Department of Polymer Materials, Vanung University, Chung-Li, Taiwan, ROC., Department of Chemical Engineering, MingChi University of Technology, Taipei, Taiwan, ROC., Department of Biotechnology, Vanung University, Chung-Li, Taiwan, ROC., Department of Biotechnology, Vanung University, Chung-Li, Taiwan, ROC; Nano Materials R&D Center, Vanung University, Chung-Li, Taiwan, ROC. Electronic address: ., Department of Chemical Engineering, National Tsing Hua University, Hsinchu, Taiwan, ROC. Electronic address: .

Abstract:  The development of stimuli-responsive materials in response to the molecules involved in biological processes has gained increased attentions. In this work, carboxymethyl chitosan (CM-chitosan) and poly(γ-glutamic acid) (pGlu) were reacted with a naturally occurring compound, genipin, leading to the formation of genipin-crosslinked CM-chitosan/pGlu conjugates with fluorescence emissions. The genipin-conjugated polymers were sensitive to the oxidation product of glucose, gluconic acid and hydrogen peroxide (H2O2). Fluorescence emissions of the polymers were quenched by gluconic acid and H2O2. An increase in the hydrodynamic diameter together with the quenching of fluorescence indicated that the genipin-conjugated polymers were self-aggregated into nanoparticles, in response to the stimulus of gluconic acid (but not for H2O2). Bovine serum albumin (BSA) could be loaded in the self-aggregated nanoparticles, and the incorporated BSA slowly released from the nanoparticles under hyper-gluconic acid conditions. This material is hence proposed as a stimuli-responsive material for optical sensing and protein delivery purposes. 

Retracted: No

PubPeer comments:
 ![file] Figure 4. ,
Time-restricted feeding without reducing caloric intake prevents metabolic diseases in mice fed a high-fat diet
Authors: Amandine Chaix
Shubhroz Gill
Mathias Leblanc
Megumi Hatori
Mark H Ellisman
Christopher Vollmers
Satchidananda Panda
James A J Fitzpatrick
Amir Zarrinpar
Matthew Joens
Luciano DiTacchio
Eric A Bushong
Journal: Cell Metabolism (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: diet-induced obesity; high-fat diet; time-restricted feeding; metabolic diseases; obesity
Affiliations: Salk Institute for Biological Studies, La Jolla, CA 92037, USA.

Abstract:  While diet-induced obesity has been exclusively attributed to increased caloric intake from fat, animals fed a high-fat diet (HFD) ad libitum (ad lib) eat frequently throughout day and night, disrupting the normal feeding cycle. To test whether obesity and metabolic diseases result from HFD or disruption of metabolic cycles, we subjected mice to either ad lib or time-restricted feeding (tRF) of a HFD for 8 hr per day. Mice under tRF consume equivalent calories from HFD as those with ad lib access yet are protected against obesity, hyperinsulinemia, hepatic steatosis, and inflammation and have improved motor coordination. The tRF regimen improved CREB, mTOR, and AMPK pathway function and oscillations of the circadian clock and their target genes' expression. These changes in catabolic and anabolic pathways altered liver metabolome and improved nutrient utilization and energy expenditure. We demonstrate in mice that tRF regimen is a nonpharmacological strategy against obesity and associated diseases. 

Retracted: No

PubPeer comments:
 Figure 1G: mice under normal or high fat diet, ad libitum or night restricted feeding eat EXACTLY the same quantity of calories per day! How is that possible? , 
 Agree with the other comment: Energy uptake under FA (ad libitum, high fat diet) and NA (ad libitum, chow diet) are similar in Figure 1 G and H. However, there is overwhelming evidence that mice fed a high fat diet ad libitum (FA) exhibit a higher energy intake than mice fed a chow diet ad libitum (NA). For example: https: doi.org 10.1016 j.cmet.2016.12.001 Figure S1A https: www.ncbi.nlm.nih.gov labs pmc articles PMC4180788 Figure 1C Could the author comment on this unexpected observation? , 
 I am not involved in this study, but not sure to entirely agree with the comments. Studies have shown before that rodents kept on high fat diet do not always increase their energy intake in the long-term (see among other examples: 18029443; 25170916; 3529988). Not sure why hyperphagia is not always present in high-fat fed rodents, but it is not completely unexpected. , 
 ![file] A quantification of the data of Fig 1B with WebPlotDigitizer shows that ad libitum mice with high fat diet are eating 7.5% more ![file] AUC ad lib: 2.880 AUC TR: 2.665 , 
 #4 Correction baseline issue): 11% more in ad libitum! ![file] ,
MicroRNA-372 enhances radiosensitivity while inhibiting cell invasion and metastasis in nasopharyngeal carcinoma through activating the PBK-dependent p53 signaling pathway
Authors: Guang-Yan Liu
Ji-Wei Mao
Fu-Guang Wang
Zai-Shuang Ju
Ruo-Yu Wang
Zhe Wang
Dong Zhou
Journal: Cancer Medicine (2019)
Discipline: CLINICAL MEDICINE
Keywords: PDZ-binding kinase; invasion; metastasis; microRNA-372; nasopharyngeal carcinoma
Affiliations: Department of Medical Oncology, Affiliated Zhongshan Hospital of Dalian University, Dalian, China., The Key Laboratory of Biomarker High Throughput Screening and Target Translation of Breast and Gastrointestinal Tumor, Dalian University, Dalian, China., College of Basic Medical Sciences, Shenyang Medical College, Shenyang, China.

Abstract:  Nasopharyngeal carcinoma (NPC) is a common cancer found in the nasopharynx, which plagues countless NPC patients. MicroRNA-372 (miR-372) has been reported to be involved in various tumors. Here, we explored the important role of miR-372 in radiosensitivity, invasion, and metastasis of NPC. Microarray analysis was conducted to search the NPC-related differentially expressed genes (DEGs) and predict the miRs regulating PBK, which suggested that miR-372 could influence the development of NPC via PBK and the p53 signaling pathway. Importantly, miR-372 was observed to target PBK, thus down-regulating its expression. Then, NPC 5-8F and C666-1 cells were selected, and treated with ionization radiation and alteration of miR-372 and PBK expression to explore the functional role of miR-372 in NPC. The expression of miR-372, PBK, Bcl-2, p53, and Bax as well as the extent of Akt phosphorylation were measured. In addition, cell colony formation, cell cycle, proliferation, apoptosis, migration, and invasion were detected. At last, tumor growth and the effect of miR-372 on radiosensitivity of NPC were evaluated. Besides, over-expressed miR-372 down-regulated Bcl-2 and PBK expression and the extent of Akt phosphorylation while up-regulated the expression of p53 and Bax. Additionally, miR-372 over-expression and radiotherapy inhibited cell clone formation, proliferation, tumor growth, migration, invasion, and cell cycle entry, but promoted cell apoptosis. However, the restoration of PBK in NPC cells expressing miR-372 reversed the anti-tumor effect of miR-372 and activation of the p53 signaling pathway. In conclusion, the study shows that up-regulated miR-372 promotes radiosensitivity by activating the p53 signaling pathway via inhibition of PBK. 

Retracted: No

PubPeer comments:
 Figs C and G,  cell cycle distribution of 5u20108F and C666u20101 cells examined by PI staining . ![file] ![file] These images are not very plausible as flow-cytometry results. The red peaks and hatched plateaux (fitted contributions of populations of cells in G1, S, G2 phases) vary in shape from panel to panel, which makes no sense. The smooth black lines - which supposedly combine those fitted contributions - bear little relationship to them. Were they hand-drawn? ,
Novel piperidine derivatives as colchicine binding site inhibitors induce apoptosis and inhibit epithelial-mesenchymal transition against prostate cancer PC3 cells
Authors: Dong-Jun Fu
Jun Li
Si-Meng Liu
Jia-Jia Yang
Journal: Journal of Enzyme Inhibition and Medicinal Chemistry (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Colchicine binding site inhibitors; apoptosis; epithelial-mesenchymal transition; piperidine.
Affiliations: Modern Research Center for Traditional Chinese Medicine, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, People’s Republic of China;, Department of Gastroenterology, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, People’s Republic of China;, Department of Pharmacy, People’s Hospital of Zhengzhou, Zhengzhou, People’s Republic of China

Abstract:  Tubulin polymerisation inhibitors that target colchicine binding site were powerful anticancer agents. Although along the years many colchicine binding site inhibitors (CBSIs) have been reported, few piperidine derivatives were identified as CBSIs. In this regard, we focussed efforts on the piperidine as a promising chemotype to develop potent CBSIs. Herein, novel piperidine derivatives were synthesised and evaluated for their antiproliferative activities. Among them, compound 17a displayed powerful anticancer activity with the IC50 value of 0.81 µM against PC3 cells, which was significantly better than 5-fluorouracil. It could inhibit tubulin polymerisation binding at the colchicine site and inhibit the tumour growth in vitro and in vivo. Further biological studies depicted that 17a suppressed the colony formation, induced apoptosis, and inhibited epithelial-mesenchymal transition against PC3 cells. These results revealed that compound 17a is a promising colchicine binding site inhibitor for the treatment of cancer and it is worthy of further exploitation. 

Retracted: No

PubPeer comments:
 Figure 3C. The wells of 0.25uM and 0.5 uM look like the same ![] ,
RETRACTED ARTICLE: Overexpression of A613T and G462T variants of DNA polymerase β weakens chemotherapy sensitivity in esophageal cancer cell lines
Authors: Xiaonan Chen
Wenqiao Zang
Min Li
Ziming Dong
Qianqian Sun
Guoqiang Zhao
Yuanyuan Wang
Journal: Cancer Cell International (2016)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Chemotherapy sensitivity; DNA polymerase β; Esophageal cancer; Mutation.
Affiliations: School of Basic Medical Sciences, Zhengzhou University, No.100 Kexue Road, 450001 Zhengzhou, Henan China., Collaborative Innovation Center of Cancer Chemoprevention of Henan, 450001 Zhengzhou, Henan China.

Abstract:  Background: Human DNA polymerase β (polβ) is a small monomeric protein that is essential for short-patch base excision repair. It plays an important role in regulating the sensitivity of tumor cells to chemotherapy. Methods: We evaluated the mutation of polβ in a larger cohort of esophageal cancer (EC) patients by RT-PCR and sequencing analysis. The function of the mutation was evaluated by CCK-8, in vivo tumor growth, and flow cytometry assays. Results: There are 229 patients with the polβ mutation, 18 patients with A613T mutation, 12 patients with G462T mutation among 538 ECs. Analysis results of survival time showed that EC patients with A613T, G462T mutation had a shorter survival than the others (P &lt; 0.05). CCK-8 and flow cytometry assays results showed the A613T, G462T EC9706 cells were less sensitive than WT cells to 5-FU and cisplatin (P &lt; 0.05). Experiments results in vivo showed that the tumor sizes of A613T and G462T group were larger than WT and polβ-/- groups (P &lt; 0.05). Conclusions: In this study, we discovered A to T point mutation at nucleotide 613 (A613T) and G to T point mutation at nucleotide 462 (G462T) in the polβ gene through 538 EC patients cohort study. A613T and G462T variant of DNA polymerase β weaken chemotherapy sensitivity of esophageal cancer. 

Retracted: Yes

PubPeer comments:
 Retracted (8th April): https: cancerci.biomedcentral.com articles 10.1186 s12935-019-0814-1  The Editor-in-Chief has retracted this article [1] because Figure 6a and 6b show overlap with Figure 4b in [2]. An investigation by Zhengzhou University has confirmed that these figures overlap. The data reported in this article are therefore unreliable. Guoqiang Zhao agrees with this retraction. Yuanyuan Wang, Xiaonan Chen, Qianqian Sun, Wenqiao Zang, Min Li, and Ziming Dong have not responded to any correspondence about this retraction. ------------------------------------------  Figure 6a and 6b show overlap with Figure 4b in [2] -  Overlap is something of an understatement. At left, Figure 6. At right, Figure 4b from  HAX-1 promotes the chemoresistance, invasion, and tumorigenicity of esophageal squamous carcinoma cells [(Sun et al 2012)] , after a diagonal flip to facilitate comparison. ![file] Some of the tumors seem to vary in size as well as in position between the two Figures, suggesting that the composition was performed digitally rather than physically. , 
 [Perhaps a systemic problem] . Journals and readers may wish to proceed with caution. ,
Cucurbitacin B Inhibits the Hippo-YAP Signaling Pathway and Exerts Anticancer Activity in Colorectal Cancer Cells
Authors: Te Zhang
Ke Xiang
Yuan Si
Yezi Wu
Ying Liu
Weiguo Zhen
Xuewen Liu
Yanting Chai
Journal: Medical Science Monitor (2018)
Discipline: CLINICAL MEDICINE
Keywords: Colorectal carcinoma; Cucurbitacin B; CRC cells; proliferation; invasion
Affiliations: Child Health Center, Shiyan Maternal and Child Health Hospital, Shiyan, Hubei, China (mainland)., Laboratory of Molecular Target Therapy of Cancer, Biomedical Research Institute, Hubei University of Medicine, Shiyan, Hubei, China (mainland)., Department of Science and Education, Gucheng People's Hospital, Hubei University of Arts and Science, Xiangyang, Hubei, China (mainland).

Abstract:  BACKGROUND Colorectal carcinoma (CRC) is one of the most frequently diagnosed malignancies. Cucurbitacin B (CuB) is a natural compound isolated from herbs and shows anticancer activity in several cancers. MATERIAL AND METHODS Here, we analyzed the eﬀects of diﬀerent CuB concentrations on the proliferative and invasive behaviors of CRC cells using MTT, clonogenic assay, Transwell invasion, and wound healing assays. Flow cytometry was performed to measure the apoptotic eﬀects of CuB on CRC cells. Western blot and real-time PCR were used to investigate the expression of apoptosis and Hippo-YAP signaling pathway proteins. RESULTS CuB inhibited the proliferation and invasion of CRC cells while promoting apoptosis. In addition, the Western blot and real-time PCR results indicated that CuB suppressed YAP expression and its downstream target genes Cyr 61 and c-Myc in CRC cells. To assess the underlying mechanism, we investigated the upstream regulating factor LATS1, and the results revealed that CuB upregulated LATS1 expression in CRC cells. CONCLUSIONS In conclusion, our findings uncovered a novel therapeutic mechanism of CuB and suggest that there is therapeutic potential and feasibility in developing novel YAP inhibitors for cancer treatment. 

Retracted: No

PubPeer comments:
 Fig 2A.  CuB inhibits the invasion and migration of CRC cells. (A) HT29 cells were pretreated with CuB for 30 min. The invasion assay was performed using modified 24-well microchemotaxis chambers. Then, randomly chosen areas were photographed (u00d7100), and the number of cells that migrated to the lower surface was counted as a percentage of invasion.  Overlap marked. ![file] ,
Galectin-1 Promotes Vasculogenic Mimicry in Gastric Cancer by Upregulating EMT Signaling
Authors: Jian Wu
Yanjun Lian
Yan Zhou
Yuanjie Wang
Qinghong Liu
Xiaolan You
Dehu Chen
Jiawen Dai
Journal: Journal of Cancer (2019)
Discipline: CLINICAL MEDICINE
Keywords: Epithelial-to-mesenchymal transition; Galectin-1; Gastric cancer; Vasculogenic mimicry.
Affiliations: Department of Gastrointestinal Surgery, Hospital Affiliated 5 to Nantong University (Taizhou People's Hospital), Taizhou, Jiangsu province, China.

Abstract:  Background: Galectin-1 (Gal-1) expression was positively associated with vasculogenic mimicry (VM) in primary gastric cancer (GC) tissue, and that both Gal-1 expression and VM in GC tissue are indicators of poor prognosis. However, whether Gal-1 promotes VM, and by what mechanismsremains unknown. Methods: To investigate the underlying mechanisms,wound healing assay, proliferation assay, invasion assay, and three-dimensional culture were used to evaluate the invasion, metastasis and promoted VM formation effects of the Gal-1. We monitored the expression level of sociated proteins in GC tissues, cell lines in vitro and nude mice tumorigenicity in vivo by immunohistochemistry and western blot. Results: Gal-1 overexpression significantly promoted the proliferation, invasion, migration, and VM formation of MGC-803 cells. Gal-1 was associated with E-cadherin and vimentin in vitro and in clinical samples. The epithelial-to-mesenchymal transition (EMT) induced in MGC-803 cells by TGF-β1 was accompanied by Gal-1 activation and promotion of VM formation, while knockdown of Gal-1 reduced the response to TGF-β1, suggesting that Gal-1 promotes VM formation by activating EMT signaling. Overexpression of Gal-1 accelerated subcutaneous xenograft growth and facilitated pulmonary metastasis in athymic mice, enhanced the expression of EMT markers, and promoted VM formation in vivo. Conclusion: Our results indicated that Gal-1 promotes VM in GC by upregulating EMT signaling; thus, Gal-1 and this pathway are potential novel targets to treat VM in GC. 

Retracted: No

PubPeer comments:
 Panels C, D, and E in Figure appear to be from the same image although these images should be from rats of different treatments. ![file] ,
A detailed quantification of differential ratings of perceived exertion during team-sport training
Authors: Matthew Weston
Shaun J McLaren
Andrew Smith
Iain R Spears
Journal: Journal of science and medicine in sport (2017)
Discipline: CLINICAL MEDICINE
Keywords: Internal load; RPE; Rugby; Training demands; Training monitoring
Affiliations: Sport & Exercise Subject Group, School of Social Sciences, Business and Law, Teesside University, UK. Electronic address: ., A S Strength and Conditioning Limited, UK; Nottingham Rugby, UK., Sport & Exercise Subject Group, School of Social Sciences, Business and Law, Teesside University, UK.

Abstract:  Objectives: To investigate the application of differential ratings of perceived exertion (dRPE) to team-sport training. Design: Single cohort, observational study. Methods: Twenty-nine professional rugby union players were monitored over a six-week intensified training period. Training sessions were classified as: high-intensity intervals, repeated high-intensity efforts, speed, skill-based conditioning, skills, whole-body resistance, or upper-body resistance. After each session, players recorded a session rating of perceived exertion (sRPE; CR100®), along with differential session ratings for breathlessness (sRPE-B), leg muscle exertion (sRPE-L), upper-body muscle exertion (sRPE-U), and cognitive/technical demands (sRPE-T). Each score was multiplied by the session duration to calculate session training loads. Data were analysed using mixed linear modelling and multiple linear regression, with magnitude-based inferences subsequently applied. Results: Between-session differences in dRPE scores ranged from very likely trivial to most likely extremely large and within-session differences amongst dRPE scores ranged from unclear to most likely very large. Differential RPE training loads combined to explain 66-91% of the variance in sRPE training loads, and the strongest associations with sRPE training load were with sRPE-L for high-intensity intervals (r=0.67; 90% confidence limits ±0.22), sRPE-B for repeated high-intensity efforts (0.89; ±0.08) and skill-based conditioning (0.67; ±0.19), sRPE-T for Speed (0.63; ±0.17) and Skills (0.51; ±0.28), and sRPE-U for resistance training (whole-body: 0.61; ±0.21, upper-body: 0.92; ±0.07). Conclusions: Differential RPE can provide a detailed quantification of internal load during training activities commonplace in team sports. Knowledge of the relationships between dRPE and sRPE can isolate the specific perceptual demands of different training modes. 

Retracted: No

PubPeer comments:
 There are recurring patterns in a flow cytometry figure (2C) that cannot be explained through chance alone.  Control appears to be a re-gating of  untreated which has been slightly nudged along the Y-axis. Do the authors have an explanation to how this may have occurred? ![file] , 
 Figure 3B, after rotation and dimensions adjusted. *** ![file] , 
 Figure 3B and Figure 5E, after rotation. *** ![file] *** ![file] , 
 Two images in Figure 3B and 5E seem to have some matching internal features. *** ![file] *** ![file] , 
 Figure 3B and Figure 5E after rotation. *** ![file] *** ![file] ,
The synthetic peptide WKYMVm attenuates the function of the chemokine receptors CCR5 and CXCR4 through activation of formyl peptide receptor-like 1
Authors: Y Le
T J Rogers
F W Ruscetti
J M Wang
J A Mikovits
W Gong
E E Henderson
M A Wetzel
B Q Li
Journal: Blood (2001)
Discipline: CLINICAL MEDICINE
Keywords: G protein-coupled receptor; STM receptor; FPRL1; HIV-1; chemokine receptors
Affiliations: Intramural Research Support Program and the Laboratory of Antiviral Drug Mechanism, NCI-Screening Technologies Branch, SAIC Frederick, MD, USA.

Abstract:  The G protein-coupled 7 transmembrane (STM) chemoattractant receptors can be inactivated by heterologous desensitization. Earlier work showed that formly peptide receptor-like 1 (FPRL1), an STM receptor with low affinity for the bacterial chemotactic peptide formyl-methionyl-leucyl-phenylalamine (fMLF), is activated by peptide domains derived from the human immunodeficiency virus (HIV)-1 envelope glycoprotein gp120 and its activation results in desensitization and down-regulation of the chemokine receptors CCR5 and CXCR4 from monocyte surfaces. This study investigated the possibility of interfering with the function of CCR5 or CXCR4 as HIV-1 coreceptors by activating FPRL1. Cell lines were established expressing FPRL1 in combination with CD4/CXCR4 or CD4/CCR5 and the effect of a synthetic peptide, WKYMVm, a potent activator of formyl peptide receptors with preference for FPRL1 was determined. Both CXCR4 and CCR5 were desensitized by activation of the cells with WKYMVm via a staurosporine-sensitive pathway. This desensitization of CXCR4 and CCR5 also attenuated their capacity as the fusion cofactors for HIV-1 envelope glycoprotein and resulted in a significant inhibition of p24 production by cell lines infected with HIV-1 that use CCR5 or CXCR4 as coreceptors. Furthermore, WKYMVm inhibited the infection of human peripheral monocyte-derived macrophages and CD4(+) T lymphocytes by R5 or X4 strains of HIV-1, respectively. These results indicate that heterologous desensitization of CCR5 and CXCR4 by an FPRL1 agonist attenuates their major biologic functions and suggest an approach to the development of additional anti-HIV-1 agents. (Blood. 2001;97:2941-2947) 

Retracted: No

PubPeer comments:
 The scope of this paper is the treatment of lice resistant to ivermectin. The authors declared no competing interests. However, according to a poster from the Institut Hospitalo-Universitaire de Marseille (see below), 1 of the author seems to be the founders of a pharmaceutical company called Arthrobac Pharma. This pharmaceutical company is dedicated to the treatment of lice using ivermectin in combination with other products. Being a founder of a pharmaceutical company dedicated to the treatment of lice may be considered as a competing interest when the article address the treatment of lices. Can the author explain if they still had any interest in this pharmaceutical company when the manuscript was submitted? ![Poster](http: backup.mediterranee-infection.com arkotheque client ihumed _depot_arko articles 579 poster_img.jpg) ,
Amazonian head lice-specific genotypes are putatively pre-Columbian
Authors: Amina Boutellis
Aurélie Veracx
Didier Raoult
Jônatas Abrahão
Journal: American Journal of Tropical Medicine and Hygiene (2013)
Discipline: CLINICAL MEDICINE
Keywords: Head lice; body lice; mitochondrial phylotypes; genotyping; Cytochrome b
Affiliations: Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes: URMITE, Aix Marseille Université, Faculté de Médecine, Marseille, France. 

Abstract:  Head and body lice are strict obligate human ectoparasites with three mitochondrial phylotypes (A, B, and C). Using molecular methods for genotyping lice (Cytochrome b and multi-spacer typing), and comparing our results with all the sequences of human lice that were genotyped previously, we assessed the presence of a specific American genotype that most likely predates the Columbian era in head lice collected from Amazonia. 

Retracted: No

PubPeer comments:
 The authors mention that: *This study was approved by the Ethic Committee of the Institute Fu00e9du00e9ratif de Recherche 48, Marseille, France (Agreement no. 12-017) and informed verbal consent was obtained from all of the participants involved here. We collected 30 head lice samples from three different states in Brazil.* In Brazil, research involving human beings is defined per [ResNo466](http: conselho.saude.gov.br resolucoes 2012 Reso466.pdf) as  research that, individually or collectively, have as a participant the human being, in its entirety or parts of it, and involve him in adirect or indirect, including the handling of your data, information or biological materials Per [ResNo466](http: conselho.saude.gov.br resolucoes 2012 Reso466.pdf), research involving human beings must be submitted to the appreciation of the local CEP or to the CONEP when relevant. Furthermore, the informed consent form must be a written document and signature must be obtained to get the participant approval (See II.23 [ResNo466](http: conselho.saude.gov.br resolucoes 2012 Reso466.pdf)). However, the authors didn t mention any approval from a local brazilian ethics committe, a CEP or the Conep. And the authors mention a verbal consent and not a written consent. The authors only mention an approval from a french local ethics committee affiliated to the institution as some of the authors. It would be in a great interest if the authors can mention the name of the Brazilian ethics committee which approved this study, the approval number, the date of the ethics approval. In the case of the authors didn t obtain an approval from an ethics committee in Brazil, can the authors explain the rationale and the reason of this waiver considering the ResNo466? ,
Estrogen receptor α-coupled Bmi1 regulation pathway in breast cancer and its clinical implications
Authors: Lin Hou
Hong Zhang
Bo Zhang
Michael A McNutt
Haijing Liu
Wei Hou
Yongxin Zou
Xin Li
Jing Zhao
Shuang Zhang
Huali Wang
Jingzhuo Mao
Journal: BMC Cancer (2014)
Discipline: CLINICAL MEDICINE
Keywords: Bmi1; ERα; HER2; breast cancer; signaling molecules
Affiliations: Department of Pathology, Health Science Center of Peking University, 38 Xueyuan Road, Haidian District, Beijing 100191, China. .

Abstract:  Background: Bmi1 has been identified as an important regulator in breast cancer, but its relationship with other signaling molecules such as ERα and HER2 is undetermined. Methods: The expression of Bmi1 and its correlation with ERα, PR, Ki-67, HER2, p16INK4a, cyclin D1 and pRB was evaluated by immunohistochemistry in a collection of 92 cases of breast cancer and statistically analyzed. Stimulation of Bmi1 expression by ERα or 17β-estradiol (E2) was analyzed in cell lines including MCF-7, MDA-MB-231, ERα-restored MDA-MB-231 and ERα-knockdown MCF-7 cells. Luciferase reporter and chromatin immunoprecipitation assays were also performed. Results: Immunostaining revealed strong correlation of Bmi1 and ERα expression status in breast cancer. Expression of Bmi1 was stimulated by 17β-estradiol in ERα-positive MCF-7 cells but not in ERα-negative MDA-MB-231 cells, while the expression of Bmi1 did not alter expression of ERα. As expected, stimulation of Bmi1 expression could also be achieved in ERα-restored MDA-MB-231 cells, and at the same time depletion of ERα decreased expression of Bmi1. The proximal promoter region of Bmi1 was transcriptionally activated with co-transfection of ERα in luciferase assays, and the interaction of the Bmi1 promoter with ERα was confirmed by chromatin immunoprecipitation. Moreover, in breast cancer tissues activation of the ERα-coupled Bmi1 pathway generally correlated with high levels of cyclin D1, while loss of its activity resulted in aberrant expression of p16INK4a and a high Ki-67 index, which implied a more aggressive phenotype of breast cancer. Conclusions: Expression of Bmi1 is influenced by ERα, and the activity of the ERα-coupled Bmi1 signature impacts p16INK4a and cyclin D1 status and thus correlates with the tumor molecular subtype and biologic behavior. This demonstrates the important role which is played by ERα-coupled Bmi1 in human breast cancer. 

Retracted: No

PubPeer comments:
 180 degree inverted duplication in last column ![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. ,
miR-451 selectively increases sensitivity to cisplatin in ERCC1-high non-small cell lung cancer cells
Authors: Hao Zhao
Kaihua Liu
Hong Tian
Yong Zhang
Kai Ma
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Retraction; miR-451; cisplatin; ERCC1-high; non-small cell lung cancer
Affiliations: Department of Thoracic Surgery, The Affiliated Hospital of Qingdao University, Qingdao 266003, China.

Abstract:  Retraction: "miR-451 selectively increases sensitivity to cisplatin in ERCC1-high non-small cell lung cancer cells" from the Journal of Cellular Biochemistry by Kaihua Liu, Hong Tian, Yong Zhang, Hao Zhao, and Kai Ma published online on 6 January 2018 in Wiley Online Library (wileyonlinelibrary.com), has been withdrawn by agreement between the journal Editor in Chief Gary S. Stein and John Wiley and Sons, Inc. The retraction has been agreed because the authors are not responding to the requests to finalize their article for publication in the journal as the Version of Record. 

Retracted: No

PubPeer comments:
 Retracted. The above article, ... published online on 6 January 2018 in Wiley Online Library (wileyonlinelibrary.com), has been withdrawn by agreement between the journal Editor in Chief Gary S. Stein and John Wiley and Sons, Inc. The retraction has been agreed because the authors are not responding to the requests to finalize their article for publication in the journal as the Version of Record. It had other issues. Fig 3: ![file] Plagiarising [a comment by Elisabeth Bik] : This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels. Despite these similarities, these papers are authored by researchers from different departments and institutes, with almost no overlap in authors. The list of these papers is available here: https: docs.google.com spreadsheets d 1KXqTAyl4j-jVorFPMD2XRpr76LcIKJ0CVyIvRj0exYQ edit?usp=sharing A more detailed description of this set of papers, suspected to all be generated by a common source, a paper mill , can be found here: - https: forbetterscience.com 2020 01 24 the-full-service-paper-mill-and-its-chinese-customers (January 2020) - https: scienceintegritydigest.com 2020 02 21 the-tadpole-paper-mill (February 2020) The same paper mill has been described in these papers: - Jana Christopher - Systematic fabrication of scientific images revealed - FEBS Letters (2018) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13201 - Jennifer A Byrne and Jana Christopher - Digital magic, or the dark arts of the 21st centuryu2014how can journals and peer reviewers detect manuscripts and publications from paper mills? - FEBS Letters (2020) - https: febs.onlinelibrary.wiley.com doi full 10.1002 1873-3468.13747 ,
RETRACTED: Involvement of Hus1 in the chain elongation step of DNA replication after exposure to camptothecin or ionizing radiation
Authors: Jun Guan
George Iliakis
Xiang Wang
Baocheng Hu
Ya Wang
Robert S Weiss
Journal: Nucleic Acids Research (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: DNA damage; S phase checkpoint; replicon initiation; chain elongation; Hus1-deficient
Affiliations: Department of Radiation Oncology, Kimmel Cancer Center of Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA.

Abstract:  DNA damage-induced S phase (S) checkpoint includes inhibition of both replicon initiation and chain elongation. The precise mechanism for controlling the two processes remains unclear. In this study, we showed that Hus1-deficient mouse cells had an impaired S checkpoint after exposure to DNA strand break-inducing agents such as camptothecin (CPT) (&gt;or=1.0 micro M), or ionizing radiation (IR) (&gt;or=15 Gy). The Hus1-dependent S checkpoint contributes to cell resistance to CPT. This impaired S checkpoint induced by CPT or IR in Hus1-deficient cells reflected mainly the chain elongation step of DNA replication and was correlated with the reduction of dissociation of PCNA from DNA replication foci. Although Hus1 is required for Rad9 phosphorylation following exposure of cells to CPT or IR, Hus1-deficient cells showed normal activation of ATR/CHK1 and ATM kinases at doses where the checkpoint defects were manifested, suggesting that Hus1 is not a component of the sensor system for activating these pathways in S checkpoint induced by CPT or IR. 

Retracted: Yes

PubPeer comments:
 Figure 4A. Much more similar than you would expect. https: imgur.com hLqGCLI , 
 Figure 4B. Much more similar than you would expect. https: imgur.com wJ3bPzK , 
 Figure 4A. Much more similar than you would expect. https: imgur.com hLqGCLI , 
 paper retracted 10.1093 nar gkaa119 https: academic.oup.com nar article 48 6 3396 5755884  In Figure 4B, multiple bands have been duplicated. While these irregularities may not fundamentally affect the results and conclusions, the Editors nonetheless note that such manipulation of data and corresponding figures is unacceptable, and request retraction of the article. ,
Leishmania (Viannia): genetic analysis of cutaneous and mucosal strains isolated from the same patient
Authors: Elisa Cupolillo
Nancy Saravia
Vivian Hernandez
Patricia Cuervo
Nedia Nehme
Octavio Fernandes
Journal: Experimental Parasitology (2004)
Discipline: MICROBIOLOGY
Keywords: Leishmania; genotypically; metastasized; mucosal; cutaneous
Affiliations: Department of Tropical Medicine, Oswaldo Cruz Institute, FIOCRUZ, Rio de Janeiro, Brazil.

Abstract:  Ten pairs of Leishmania (Viannia) strains isolated from mucosal and cutaneous lesions of the same patient were analyzed genotypically in order to determine whether populations that had metastasized to mucosal sites differed from those in the cutaneous lesion. The strains were previously characterized by multi locus enzyme electrophoresis and/or monoclonal antibodies reactivity, and, for this study, only isolates from the same patient which were identified as the same species were employed. PCR-RFLP of internal transcribed spacer (ITS) rDNA, random amplified polymorphic DNA (RAPD), and schizodeme analyses were conducted. All genotyping methods revealed microheterogeneity between cutaneous and mucosal isolates from the same patient. The PCR-RFLP of the ITS rDNA and RAPD analysis were numerically analyzed through similarity coefficients and dendrograms were generated. All phenograms clustered cutaneous and mucosal strains of the same patient in one branch with a high degree of similarity, and phenetic analysis matched between them. Schizodeme analysis revealed differences between strains that composed some pairs. Genetic analyses indicate that some populations that metastasize to mucosal sites are distinguishable from the population in cutaneous lesions, however, other approaches will be required to associate genetic polymorphisms with the cutaneous or mucosal phenotype of strains. 

Retracted: No

PubPeer comments:
 Figure 1. * Red boxes: The 1377C and 1377M lanes in Figure 1A look remarkably similar. * Blue boxes: The 1377C and 1377M lanes in Figure 1C look remarkably similar. ![file] ,