PReD-Bench/PRed-Bench huggingface dataset:
Ets family protein, erg expression in developing and adult mouse tissues by a highly specific monoclonal antibody
Authors: Ahmed A Mohamed
Isabell A Sesterhenn
Shiv Srivastava
Sathibalan Ponniah
Valeri Vasioukhin
Charles J Bieberich
Natallia Mikhalkevich
Taduru L Sreenath
Shyh-Han Tan
Albert Dobi
Journal: Journal of Cancer (2010)
Discipline: CLINICAL MEDICINE
Keywords: Development.; ERG; ERG MAb; Ets Related Gene; Expression
Affiliations: 1. Center For Prostate Disease Research, Department of Surgery, United States Military Cancer Institute, Uniformed Services University of the Health Sciences, Bethesda MD 20814, USA.

Abstract:  Oncogenic activation of the ETS Related Gene (ERG) in humans was originally identified in subsets of Ewing sarcomas, myeloid leukemias and, recently, in the majority of prostate cancers. Expression of human ERG protein and consequently its functions in normal and disease states needs to be better understood in light of its suggested role in cell differentiation and proliferation. Here, we analyzed temporal and spatial expression of the Erg (mouse protein) by immunohistochemical analysis during mouse embryonic and adult organogenesis using a highly specific ERG monoclonal antibody (ERG MAb). This study establishes widespread immunolocalization of Erg protein in endothelial cells and restricted expression in precartilage and hematopoietic tissues. Intriguingly, Erg is not expressed in any epithelial tissue including prostate epithelium, or in infiltrating lymphocytes that are occasionally seen in the prostate environment, a common site of tumors with ERG rearrangements and unscheduled ERG expression. These findings will further aid in investigations of Erg functions in normal and disease conditions. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Semaphoring 4D is required for the induction of antioxidant stress and anti-inflammatory effects of dihydromyricetin in colon cancer
Authors: Fei Wang
Pengfei Zhang
Jun Liang
Xuemei Zhang
Jing Wu
Journal: International Immunopharmacology (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: Colorectal cancer; Dihydromyricetin; Inflammation; Oxidative stress; Semaphorin 4D.
Affiliations: Oncology Medicine Center, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China., Department of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China., Department of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China. Electronic address: .

Abstract:  Semaphorin 4D (Sema4D) has been involved in cancer progression, the expression of which is associated with the poor clinical outcomes of some cancer patients. Dihydromyricetin (DMY) has antitumor potentials for different types of human cancer cells. However, the pharmacological effects of DMY on colon cancer (CC) or the regulatory effects of Sema4D on this process remain largely unknown. In the present study, we aimed to evaluate the effects of DMY on CC, and to elucidate the role of Sema4D in DMY-induced antitumor effects. DMY inhibited the proliferation and growth of Colo-205 colon cancer cells significantly in vivo and in vitro. DMY inhibited reactive oxygen species (ROS) and malondialdehyde (MDA) levels, but increased glutathione (GSH) level. Moreover, the activities of antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and heme oxygenase 1 (HO-1) were enhanced by DMY treatment in vitro, showing strong anti-oxidative stress effect. In addition, DMY inhibited the secretion of interleukin 1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor (TNF-α) in the supernatant of Colo-205 culture medium. Besides, the expressions of cyclooxygenase (COX-2) and inducible nitric oxide synthase (iNOS) were suppressed by DMY in dose-dependent manners in vivo, showing potent anti-inflammatory effect. Further investigations showed that DMY suppressed the expression and secretion of Sema4D in Colo-205 cells and tissues. Interestingly, overexpression of Sema4D significantly weakened the regulatory effects of DMY on oxidative stress. Furthermore, overexpression of Sema4D significantly attenuated the anti-inflammatory effects of DMY. Collectively, we drew a conclusion that the anti-colon cancer effect of DMY was attributed to its negative modulation on oxidative stress and inflammation via suppression of Sema4D. The findings broaden the width and depth of molecular mechanisms involved in the DMY action, facilitating the development of DMY in anti-colon cancer therapies. 

Retracted: No

PubPeer comments:
 A typo in the first word of the title: it should be Semaphorin 4D This is most likely caused by the Microsoft Word auto correct function. This  Semaphoring typo is now in many recent articles on semaphorin proteins genes. I think the typo should be corrected if it is in a title. ,
Increased expression of P-glycoprotein is associated with doxorubicin chemoresistance in the metastatic 4T1 breast cancer model
Authors: Kamilah Jackson
Lili Bao
Krzysztof Moroz
Srikanta Dash
Aliyya Haque
Rachna Jetly
Sidhartha Hazari
Journal: American Journal Of Pathology (2011)
Discipline: CLINICAL MEDICINE
Keywords: drug resistance; breast cancer; chemoresistance mechanism; metastatic 4T1; cell proliferation
Affiliations: Department of Pathology and Laboratory Medicine, Tulane University Health Sciences Center, New Orleans, Louisiana, USA.

Abstract:  Development of drug resistance is one of the major causes of breast cancer treatment failure. The goal of this study was to understand the chemoresistance mechanism using the highly metastatic 4T1 breast cancer model, which emulates stage IV breast cancer in humans. The metastatic 4T1 breast cancer cell line treated with either doxorubicin or 5-FU showed a concentration-dependent reduced cell proliferation, with induced G2-phase growth arrest (doxorubicin) or G1-phase growth arrest (5-FU). Doxorubicin treatment partially suppressed the multiorgan metastasis of 4T1 breast cancer cells in the lung, heart, liver, and bone, compared with either 5-FU or cyclophosphamide. We isolated and characterized 4T1 breast cancer cells from doxorubicin-resistant metastatic tumors (cell line 4T1-R). Multiorgan metastasis of drug-resistant 4T1 breast tumors was totally resistant to doxorubicin treatment. Our results indicate that doxorubicin is localized exclusively in the cytoplasm of resistant 4T1 breast cancer cells and that it cannot reach the nucleus because of increased nuclear expression of P-glycoprotein. Pretreatment of doxorubicin-resistant 4T1-R breast cancer cells with verapamil, a general inhibitor of P-glycoprotein, increased nuclear translocation of doxorubicin and cellular cytotoxicity. Thus, impaired nuclear translocation of doxorubicin due to increased expression of P-glycoprotein is associated with doxorubicin resistance of highly metastatic 4T1 breast cancer. 

Retracted: No

PubPeer comments:
 The resolution of the published gel images is fairly grainy. Several features in bands and lanes appear more similar than expected, and there appears to be multiple splicing between lanes. Could the authors please provide high-resolution images of the gels used in Figure 1 prior to labeling to clarify these queries. Figure 1 https: imgur.com a HiwHzX4 ,
siRNA‐mediated NCAM1 gene silencing suppresses oxidative stress in pre‐eclampsia by inhibiting the p38MAPK signaling pathway
Authors: Xiao-Lin Zhang
Feng-Xian Xu
Xiao-Yun Han
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: invasion; migration; neural cell adhesion molecule 1; oxidative stress; p38 mitogen-activated protein kinase signaling pathway
Affiliations: Department of Obstetrics, Zoucheng Hospital District of Affiliated Hospital of Jining Medical University, Zoucheng, People's Republic of China., Department of Obstetrics, Affiliated Hospital of Jining Medical University, Jining, People's Republic of China.

Abstract:  Pre-eclampsia (PE), whose pathophysiology and etiology remain undefined, represents a leading consequence of fetal and maternal mortality and morbidity. Oxidative stress (OS) is recognized to involve in this disorder. In this study, we hypothesized that neural cell adhesion molecule 1 (NCAM1) gene silencing would suppress the OS in the pregnancy complicated by PE. Initially, clinical samples were collected for determination of NCAM1 expression in placental tissues and levels of OS products in blood. To assess the regulatory mechanism of NCAM1 knockdown on OS, we used small interfering RNA (siRNA) to silence NCAM1 expression in human umbilical vein endothelial cells (HUVECs). Next, cells were treated with or without hypoxia/reoxygenation to observe the level changes of OS products and p38 mitogen-activated protein kinase (p38MAPK) pathway-related genes. Finally, an evaluation of HUVEC migration and invasion abilities was conducted by wound-healing and transwell assays. Placenta of pregnancy with PE presented significantly increased NCAM1 expression in comparison to placenta of normal pregnancy. Meanwhile, enhanced OS in blood of pregnant women with PE was observed relative to women with normal pregnancy. siRNA-mediated knockdown of NCAM1 gene could inhibit the p38MAPK signaling pathway, repress OS, and promote cell migration and invasion in HUVECs, indicating that NCAM1 inhibition could reduce the influence of PE. Importantly, blocking the p38MAPK signaling pathway reversed the inhibitory role of NCAM1 gene silencing on PE. Collectively, this study defines potential role of NCAM1 gene silencing as a therapeutic target in PE through inhibiting OS and enhancing HUVEC migration and invasion by disrupting the p38MAPK signaling pathway. 

Retracted: No

PubPeer comments:
 I am questioning the conclusion from this article due to Figure 3B and Figure 4A. Figure 3B: The presented Western blots are diffuse, and when increasing the contrast you see that the background is very different from a typical Western blot. Figure 4A: The wound-healing assay presented. is meaningless. The quality is very poor, making it impossible to conclude from the data provided. , 
 Here are the illustrations: ![file] ![file] ,
Retracted : MicroRNA‐29a inhibits proliferation and motility of schwannoma cells by targeting CDK6
Authors: Shaofeng Shui
Lei Yan
Xinwei Han
Dong Guo
Huifeng Yuan
Tengfei Li
Ji Ma
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: CDK6; JNK; miR-29a; p38MAPK/ERK; schwannoma cells.
Affiliations: Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Abstract:  MicroRNA-29 (miR-29) family is involved in various types of cancer regulation. Although miR-29 family was shown to play an inhibitory role in tumorigenesis, the effect of miR-29a expression on schwannoma cells still remains unclear. In this study, we aimed to explore the role of miR-29 family in schwannoma. The expressions of miR-29a, miR-29b, and miR-29c were detected in the Schwann tissues and cell lines using qRT-PCR. The effect of miR-29a, miR-29b, and miR-29c on cell viability, migration, invasion, and apoptosis was tested. Then, the regulatory relationship between miR-29a and CKD6 was detected using qRT-PCR, Western blot, and luciferase assay. Finally, the phosphorylation levels of mainly factors in JNK and p38MAPK/ERK pathways were analyzed by Western blot. The expression of miR-29a, miR-29b, and miR-29c was downregulated in Schwann tissues and cell lines. Cell viability, migration, invasion were decreased, while apoptosis was increased when miR-29a, miR-29b, and miR-29c overexpression. We further found that miR-29a negatively regulated expression of CDK6. Then, knockdown of miR-29a promoted cell viability, migration, invasion, and inhibited apoptosis in schwannoma cells by upregulating CDK6 expression. In addition, the overexpression of miR-29a downregulated CDK6 expression by deactivation of JNK and p38MAPK/ERK pathways. Our data suggested that miR-29a could play an important role in inhibiting proliferation and motility of cancerous Schwann cells, and may suppress tumor growth through upregulation of CDK6. 

Retracted: Yes

PubPeer comments:
 this article was found to contain falsified data and the author resigned after federal investigation but strangely the author was allowed to retract a figure rather than having then paper retracted https: www.sciencemag.org news 1999 06 emf-researcher-faked-data https: archive.nytimes.com www.nytimes.com library national science 072499sci-fake-data.html  In an agreement signed by Liburdy and ORI acting director Chris Pascal, Liburdy agreed to retract the tainted figures in the two papers  Federal officials say Liburdy did not spend all of the $3.3 million in grant money, and that the remainder is controlled by the Lawrence Berkeley Lab.  It s being used for other science and none of it has been returned to the federal government, Woods said Friday. ,
Prokaryotic ubiquitin-like ThiS fusion enhances the heterologous protein overexpression and aggregation in Escherichia coli
Authors: Sujuan Yuan
Zheng Yan
Nan Wang
Ying Ge
Jian Xu
Guohua Du
Journal: PloS one (2013)
Discipline: Multidisciplinary
Keywords: Fusion tags; Ubiquitin; SUMO; ThiS; prokaryotic expression
Affiliations: Chinese Academy of Medical Sciences and Peking Union Medical College, Institute of Materia Medica, Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study, Beijing, People's Republic of China.

Abstract:  Fusion tags are commonly employed to enhance target protein expression, improve their folding and solubility, and reduce protein degradation in expression of recombinant proteins. Ubiquitin (Ub) and SUMO are highly conserved small proteins in eukaryotes, and frequently used as fusion tags in prokaryotic expression. ThiS, a smaller sulfur-carrier protein involved in thiamin synthesis, is conserved among most prokaryotic species. The structural similarity between ThiS and Ub provoked us into expecting that the former could be used as a fusion tag. Hence, ThiS was fused to insulin A and B chains, murine Ribonuclease Inhibitor (mRI) and EGFP, respectively. When induced in Escherichia coli, ThiS-fused insulin A and B chains were overexpressed in inclusion bodies, and to higher levels in comparison to the same proteins fused with Ub. On the contrast, ThiS fusion of mRI, an unstable protein, resulted in enhanced degradation that was not alleviated in protease-deficient strains. While the degradation of Ub- and SUMO-fused mRI was less and seemed protease-dependent. Enhanced degradation of mRI did not occur for the fusions with half-molecules of ThiS. When ThiS-tag was fused to the C-terminus of EGFP, higher expression, predominantly in inclusion bodies, was observed again. It was further found that ThiS fusion of EGFP significantly retarded its refolding process. These results indicated that prokaryotic ThiS is able to promote the expression of target proteins in E. coli, but enhanced degradation may occur in case of unstable targets. Unlike eukaryotic Ub-based tags usually increase the solubility and folding of proteins, ThiS fusion enhances the expression by augmenting the formation of inclusion bodies, probably through retardation of the folding of target proteins. 

Retracted: Yes

PubPeer comments:
 Figure 2b shows the C-alpha RMSF plot. How does the residue number become 10000? As the protein is a pentamer of a 75 residue monomeric subunit, the total number of C-alpha should be (75x5) = 375. How do the authors justify the RMSF calculation? ![file] , 
 In Figure 3, the authors represent cross-correlation analyses of C-alpha atoms. Again, how the number of C-alpha atom reaches more than 900? The pentameric structure of the protein contains 375 residues which correspond to 375 C-alpha atoms. ![file] ,
Retraction : HCFU inhibits cervical cancer cells growth and metastasis by inactivating Wnt/β‐catenin pathway
Authors: Shanshan Wang
Hua Liu
Huazhen Han
Ping Liu
Shuying Ma
Journal: Journal of Cellular Biochemistry (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: 1-hexylcarbamoyl-5-fluorouracil (HCFU); Wnt/β-catenin pathway; cervical cancer; metastasis; proliferation.
Affiliations: Department of Obstetrics and Gynecology, Jining No. 1 People's Hospital, Jining 272011, China.

Abstract:  Background: 1-hexylcarbamoyl-5-fluorouracil (HCFU), also known as carmofur, is an effective chemotherapeutic agent applied to several cancers. This study was aimed to explore the functional effects of HCFU on cervical cancer cells and tried to uncover its possible mechanism. Methods: Two immortalized cervical cancer cell lines (HeLa and Caski) and primary cervical cancer cells prepared from two cervical cancer patients were used in this study. Cell viability, apoptosis, colony formation, migration, invasion, and the expressions of cell growth- and metastasis-associated factors were respectively assessed following 0-1 µg/mL of HCFU treatment for 0-48 h. Besides, the expressions of main factors in Wnt/β-catenin signaling pathway were detected following HCFU administration. Results: As a result, HCFU significantly suppressed HeLa and Caski cells viability but promoted apoptosis, both in time- and dose-dependent manner (P &lt; 0.05 or P &lt; 0.01). Besides, HCFU reduced these two cell lines colony formation capacity, migration and invasion (P &lt; 0.05, P &lt; 0.01 or P &lt; 0.001). In primary cervical cancer cells, cell viability was reduced (P &lt; 0.05 or P &lt; 0.01), the expressions of Cyclin D1, MMP2 and MMP9 were down-regulated, while the expression of E-Cadherin was up-regulated after HCFU treatment. Further, HCFU down-regulated the expressions of intranuclear β-catenin, c-Myc, and TCF-1, but has no impacts on intracytoplasmic β-catenin expression in HeLa cells and primary cervical cancer cells. Conclusion: This study demonstrated an anti-growth and anti-metastasis role of HCFU in cervical cancer cells. HCFU suppressed cervical cancer possibly via blocking Wnt/β-catenin signaling pathway. This article is protected by copyright. All rights reserved. 

Retracted: No

PubPeer comments:
 The above article, from Journal of Cellular Biochemistry, u201cHCFU inhibits cervical cancer cells growth and metastasis by inactivating Wnt u03b2u2010catenin pathwayu201d by Ping Liu, Shuying Ma, Hua Liu, Huazhen Han, and Shanshan Wang published online on 12 December 2017 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 requests to finalize their article for publication in the journal as the Version of Record. Archived copies indicate that the paper was another product of the  Tadpole Papermill . ![file] ,
Oligomeric forms of bacterial malate dehydrogenase: a study of the enzyme from the phototrophic non-sulfur bacterium Rhodovulum steppense A-20s
Authors: Marina I Falaleeva
Ilya Y Toropygin
Maya S Lyashchenko
Alexander T Eprintsev
Abir U Igamberdiev
Journal: Bioscience Biotechnology and Biochemistry (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MDH: malate dehydrogenase; Malate dehydrogenase; OAA: oxaloacetate; Rhodovulum steppense; SOD: superoxide dismutase
Affiliations: Department of Biochemistry and Cell Physiology, Voronezh State University, Voronezh, Russia, V.I. Orekhovich Research Institute of Biomedical Chemistry, Moscow, Russia, Department of Biology, Memorial University of Newfoundland, St. John’s, Canada

Abstract:  Malate dehydrogenase (EC 1.1.1.37) was purified to homogeneity from the phototrophic purple non-sulfur bacterium Rhodovulum steppense A-20s. According to gel-chromatography and electrophoretic studies, malate dehydrogenase is present as a dimer, tetramer and octamer depending on cultivation conditions. In phototrophic aerobic conditions only the tetrameric form was present, in chemotrophic aerobic conditions all three forms were detected, while in the absence of oxygen the octameric form disappeared. The malate dehydrogenase oligomers are encoded by a single gene and composed of the same 35 kDa polypeptide but differ in pH and temperature optimum, in affinities to malate, oxaloacetate, NADH and NAD+ and in regulation by cations and citrate. By modulating the cultivation conditions, it has been established that the dimer participates in the glyoxylate cycle; the tetramer operates in the tricarboxylic acid cycle, and the octamer may be involved in the adaptation to oxidative stress. 

Retracted: No

PubPeer comments:
 Fig. 1 vs Fig. 5 https: imgur.com a caVajf3 ,
LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanoma
Authors: Wenqiao Zang
Jianbo Wu
Qianqian Sun
Guoqiang Zhao
Xiaonan Chen
Lindong Zhao
Yanping Wei
Yuanyuan Wang
Journal: Medical Oncology (2016)
Discipline: CLINICAL MEDICINE
Keywords: FOXM1; LncRNA UCA1; Melanoma; miR-507.
Affiliations: Department of Dermatology, The People's Hospital of Jiaozuo City, Jiaozuo, 454000, Henan, China., School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China., School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China. ., Collaborative Innovation Center of Cancer Chemoprevention, Zhengzhou, 450001, Henan, China. .

Abstract:  Recently, the incidence of melanoma has been on the rise. Patients with distant metastasis share poor prognosis. Increasing studies have been conducted to clarify the molecular mechanisms as well as to investigate potential effective therapeutic targets in the development of melanoma. This study focuses on the LncRNA UCA1 and its downstream regulated factors. In our experiments, UCA1 expression was discovered to be upregulated in melanoma tissues and cells, while the depletion of UCA1 led to the inhibition of cell proliferation, invasion and cell cycle arrest. To further our understanding of the mechanisms of UCA1, a system of experiments was built. We found that miR-507 could directly bind to UCA1 at the miRNA recognition site, and that there was a negative correlation between miR-507 and UCA1. Additionally, FOXM1 is a target of miR-507 and can be downregulated by either miR-507 overexpression or UCA1 depletion. Downregulated FOXM1 was analogous to the depletion of UCA1 and the overexpression of miR-507. These results, taken together, provide evidence for a novel UCA1 interaction regulatory network in tumorigenesis of melanoma. 

Retracted: No

PubPeer comments:
 [Bottom]:  Figure 2 ... d transwell assay was performed in UCA1 downregulated cells to investigate changes in cell invasiveness. Apparent image reuse with [Top]:  Fig. 5. Upregulation of miR-203 decreases CRC cell invasion. Cell invasion assay was conducted to evaluate the invasive ability of HT-29 and Caco-2 cells. The images show the number of invasive cells. From  Sodium Butyrate Upregulates miR-203 Expression to Exert Anti-Proliferation Effect on Colorectal Cancer Cells [(Han et al 2016)] . ![file] , 
 [Perhaps a systemic problem] . Journals and readers may wish to proceed with caution. ,
The gastropod shell has been co-opted to kill parasitic nematodes
Authors: R Rae
Journal: Scientific Reports (2017)
Discipline: Multidisciplinary
Keywords: Exoskeletons; Gastropoda; Shell; Conchiolin; Calcium carbonate
Affiliations: Liverpool John Moores University, School of Natural Sciences and Psychology, Byrom Street, Liverpool, L33AF, UK. .

Abstract:  Exoskeletons have evolved 18 times independently over 550 MYA and are essential for the success of the Gastropoda. The gastropod shell shows a vast array of different sizes, shapes and structures, and is made of conchiolin and calcium carbonate, which provides protection from predators and extreme environmental conditions. Here, I report that the gastropod shell has another function and has been co-opted as a defense system to encase and kill parasitic nematodes. Upon infection, cells on the inner layer of the shell adhere to the nematode cuticle, swarm over its body and fuse it to the inside of the shell. Shells of wild Cepaea nemoralis, C. hortensis and Cornu aspersum from around the U.K. are heavily infected with several nematode species including Caenorhabditis elegans. By examining conchology collections I show that nematodes are permanently fixed in shells for hundreds of years and that nematode encapsulation is a pleisomorphic trait, prevalent in both the achatinoid and non-achatinoid clades of the Stylommatophora (and slugs and shelled slugs), which diverged 90-130 MYA. Taken together, these results show that the shell also evolved to kill parasitic nematodes and this is the only example of an exoskeleton that has been co-opted as an immune system. 

Retracted: No

PubPeer comments:
 Actually, no one can found parasitic liked things in the dead shells and even fossils. It can not be found where the author mentioned. It only can be found in the mantle of the terrestrial Gastropoda. ,
RETRACTED: Autoimmunity as the Consequence of a Spontaneous Mutation in Rasgrp1
Authors: David Beier
Janet Buhlmann
Stacey L Stang
Alessio Nencioni
Wei Hu
Adam Schmucker
James C Stone
Timothy Chevassut
Roderick T Bronson
Nancy A Dower
Satoshi Takamatsu
Andrey N Antov
Bing Lim
Luk Van Parijs
Keith B Elkon
Guosheng Lin
Katrin Layer
Xiaoyu Li
Journal: Immunity (2003)
Discipline: IMMUNOLOGY
Keywords: mouse strain; recessive genetic lesion; lymphoproliferative autoimmune syndrome; systemic lupus erythematosus; Rasgrp1

Abstract:  A mouse strain was identified with a recessive genetic lesion, which spontaneously developed a lymphoproliferative autoimmune syndrome exhibiting features of systemic lupus erythematosus. Positional mapping of the disease-associated locus revealed a lesion in Rasgrp1 that prevented the translation of the RasGRP1 protein. T cells from these mice failed to activate Ras or proliferate vigorously following antigen encounter and showed defects in positive selection. Peripheral RasGRP1lag T cells spontaneously adopted a memory phenotype and were able to transfer disease to lymphopenic recipient mice. CD4+ T cells accumulated in the lymphoid tissues of older RasGRP1lag mice and were resistant to activation-induced cell death. RasGRP1lag B cells were functionally normal, but activated B cells were detected in older mice, as were autoantibodies directed against self-antigens. Our findings indicate that Ras signaling pathways are required to maintain T cell tolerance and to prevent autoimmune disease. 

Retracted: No

PubPeer comments:
 2012 retraction. https: www.cell.com immunity fulltext S1074-7613(12)00191-4?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1074761312001914%3Fshowall%3Dtrue The authors have agreed to retract the paper because of the falsification of the Western blot in Figure 6A. The figure shows a defect in Ras activation, labeled as RasGTP, following TCR engagement, in thymocytes isolated from a RasGRP1 lag mutant mouse strain. This data set is one of several that show signaling and functional deficiencies identified for cells with lost of function of RasGRP. The authors stand by the validity of the other figures, results, and interpretation in this paper. This matter was investigated by the Massachusetts Institute of Technology and the Office of Research Integrity at the United States Department of Health Human Services, which found that the figure was falsified by Luk Van Parijs, who is solely responsible. The authors deeply regret any inconvenience resulting from the publication of this data. , 
 https: retractionwatch.com 2012 05 30 an-immunity-retration-for-luk-van-parijs-three-years-after-the-ori-found-evidence-of-fabrication-in-the-paper 5 retractions. http: retractiondatabase.org RetractionSearch.aspx#?auth%3dVan%2bParijs%252c%2bLuk ,
Apoptotic death in Leishmania donovani promastigotes in response to respiratory chain inhibition: complex II inhibition results in increased pentamidine cytotoxicity
Authors: Chandrima Shaha
Ashish Mehta
Journal: Journal of Biological Chemistry (2004)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: respiratory chain inhibition; cell death; Leishmania spp.; apoptosis; mitochondrial hyperpolarization
Affiliations: National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi 110067, India.

Abstract:  The biochemical changes consequent to respiratory chain inhibition and their relationship to cell death in Leishmania spp. remain elusive. Inhibitors of respiratory chain complexes I, II, and III were able to induce apoptotic death of the bloodstream form of Leishmania donovani. Complex I inhibition resulted in mitochondrial hyperpolarization that was preceded by increased superoxide production. Limitation of electron transport by thenoyltrifluoroacetone and antimycin A, inhibitors of complexes II and III, respectively, resulted in dissipation of mitochondrial membrane potential that was sensitive to cyclosporin A, a blocker of mitochondrial permeability transition pore. Further studies conducted with thenoyltrifluoroacetone showed maximal generation of hydrogen peroxide with a moderate elevation of superoxide levels. Complex III inhibition provoked superoxide generation only. Interference with complex II but not complexes I and III increased intracellular Ca(2+). A tight link between Ca(2+) and reactive oxygen species was demonstrated by antioxidant-induced diminution of the Ca(2+) increase. However, chelation of extracellular Ca(2+) could not abrogate the early increase of reactive oxygen species, providing evidence that Ca(2+) elevation was downstream to reactive oxygen species generation. Ca(2+) influx occurred through nonselective cation and L-type channels and Na(+)/Ca(2+) exchanger-like pathways. Antioxidants such as glutathione and Ca(2+) channel blockers reduced apoptotic death. This study provides a new possibility that concurrent inhibition of respiratory chain complex II with pentamidine administration increases cytotoxicity of the drug. This increased cytotoxicity was connected to a 4-fold elevation in intracellular Ca(2+) that was pooled only from intracellular sources. Therefore, inhibition of complexes I, II, and III leads to apoptosis and complex II inhibition in parallel with pentamidine administration-enhanced drug efficacy. 

Retracted: No

PubPeer comments:
 The authors in this paper developed a very complicated and unconventional decision making method for evaluation of hydrogen refueling stations in China. However, the proposed method itself is confusing and the numerical results presented are not convincing. For example, consider the factor $B_{11}$ in **Table 4**, the author provided the values as $$D=0.334$$ $$R=0.171$$ It is clear that given these two values, $$D-R = 0.334-0.171=0.163$$ However, the authors claimed that the value of $D-R$ is $$-0.163$$ Could the authors address this issue? ![file] ,
Increased NHE1 expression is targeted by specific inhibitor cariporide to sensitize resistant breast cancer cells to doxorubicin in vitro and in vivo
Authors: Fan Feng
Qi Chen
Hui Yang
Xiao-Lan Zhu
Yueqin Liu
Wenlin Xu
Journal: BMC Cancer (2019)
Discipline: CLINICAL MEDICINE
Keywords: Cariporide; Chemotherapy; MCF-7/ADR; MDR; NHE-1

Abstract:  Background: The Na+/H+ exchanger (NHE1) plays a crucial role in cancer cell proliferation and metastasis. However, the mechanism underlying chemotherapeutic resistance in cancer cells has not been completely elucidated. The NHE1 inhibitor cariporide has been demonstrated to inhibit human cancer cell lines. The goal of this study was to provide new sights into improved cancer cell chemosensitivity mediated by cariporide with activation of the apoptosis pathway. Methods: The NHE1 expression levels were first evaluated using the online database Oncomine and were determined by RT-PCR and western blot in vitro and in vivo. Cell proliferation was assessed In vitro through a CCK-8 assay, and apoptosis was analyzed by flow cytometry. An in vivo analysis was performed in BALB/c nude mice, which were intraperitoneally injected with MCF-7/ADR cells. Results: NHE1 levels were significantly higher in breast cancer tissue than adjacent tissue, as well as in resistant cancer cells compared to sensitive cells. Cariporide induced the apoptosis of MCF-7/ADR cells and was associated with the intracellular accumulation of doxorubicin and G0/G1 cell cycle arrest. Moreover, cariporide decreased MDR1 expression and activated cleaved caspase-3 and caspase-9, promoting caspase-independent apoptosis in vitro. In vivo, cariporide significantly improved doxorubicin sensitivity in a xenograft model, enhancing tumor growth attenuation and diminishing tumor volume. Conclusions: Our results demonstrate that cariporide significantly facilitates the sensitivity of breast cancer to doxorubicin both in vitro and in vivo. This finding suggests that NHE1 may be a novel adjuvant therapeutic candidate for the treatment of resistant breast cancer. 

Retracted: No

PubPeer comments:
 Two Flow cytometry dot plots in Figure 3B share too many data points in one specific area (Adr vs CP + Adr). ![file] ,
Follicle stimulating hormone and estradiol alter immune response in osteoarthritic mice in an opposite manner
Authors: Nina Ivanovska
Ralitsa Zhivkova
Lyudmila Belenska-Todorova
Maya Markova
Journal: International Journal of Immunopathology and Pharmacology (2021)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: 17β-estradiol; collagenase-induced osteoarthritis; follicle stimulating hormone; osteoblasts; osteoclasts.
Affiliations: Department of Biology, Medical Genetics and Microbiology, Sofia University, Medical Faculty, Sofia, Bulgaria, Department of Biology, Medical Faculty, Medical University-Sofia, Sofia, Bulgaria, Department of Immunology, Institute of Microbiology, Bulgarian Academy of Sciences, Sofia, Bulgaria

Abstract:  Although a number of studies have shown that the occurrence and progression of osteoarthritis (OA) is related to endocrine system dysfunction, there is limited evidence about what roles sex hormones play. The aim of the present study was to examine the capacity of 17β-estradiol (ED) and follicle stimulating hormone (FSH) to alter the differentiation of bone marrow (BM) cells in arthritic mice. The experiments were conducted in collagenase-induced osteoarthritis in mice. Cartilage degradation was observed by safranin and toluidine blue staining. Flow cytometry was used to define different BM and synovial cell populations. The influence of FSH and ED on osteoclastogenesis was studied in BM cultures and on the osteoblastogenesis in primary calvarial cultures. The levels of IL-8, TNF-α, FSH, and osteocalcin were estimated by ELISA. FSH increased cartilage degradation and serum osteocalcin levels, while ED abolished it and lowered serum osteocalcin. FSH elevated the percentage of monocytoid CD14+/RANK+ and B cell CD19+/RANK+ cells in contrast to ED which inhibited the accumulation of these osteogenic populations. Also, ED changed the percentage of CD105+/F4/80+ and CD11c+ cells in the synovium. FSH augmented and ED suppressed macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast (OC) formation, and this correlated with a respective increase and decrease of IL-8 secretion. FSH did not influence osteoblast (OB) formation while ED enhanced this process in association with changes of TNF-α, IL-8, and osteocalcin production. ED reduced osteoclast generation in bone. The key outcome of the current study is that both hormones influenced BM cell differentiation, with FSH favoring osteoclast formation and ED favoring osteoblast accumulation. 

Retracted: No

PubPeer comments:
 In Figure 2M, there appear to be some sample images used more than once. *** Original 2M ![file] *** 2M enhanced contrast ![file] *** Full figure ![file] , 
 The authors have advised due to an error that occurred inadvertently at the time of figure assembly, Figure 2M on page 3956 is incorrect. The correct Figure 2 is shown below. The authors have also advised there is an error in Figure 3 on page 3960. The concentration units in part B show u201cmgu201d theyshould read u201cmg mlu201d. The correct Figure 3 is shown below. The authors apologize for these errors. ![file] ![file] ![file] ,
Far reach of Fusobacterium nucleatum in cancer metastasis
Authors: Ye Yang
Christian Jobin
Journal: Gut (2020)
Discipline: CLINICAL MEDICINE
Keywords: bacterial infection; cancer.
Affiliations: Medicine, University of Florida, Gainesville, Florida, USA ., Department of Medicine, University of Florida College of Medicine, Gainesville, Florida, USA.

Abstract: Approximately 8 years ago, two groups independently reported enrichment of Fusobacterium nucleatum (Fn) in human colorectal cancer (CRC) tissues compared with adjacent normal tissues.1 2 Since this discovery, intense research interests have been drawn to the bacterium in the context of CRC. The association between Fn and CRC has been confirmed in numerous studies, and several Fn-driven pro-oncogenic mechanisms have been proposed based on observations from preclinical models.3 Notably, much of our knowledge regarding the involvement of Fn is at the primary CRC development stage. How Fn might impact CRC metastasis—the late stage of carcinogenesis that really determines poor prognosis in patients—is relatively unexplored, despite detection of the bacterium in CRC metastases to the liver and lymph nodes.1 2 4 The first evidence that Fn is important for CRC metastasis emerged in 2017, when it was shown that Fn presence correlated with successful establishment of CRC patients-derived xenografts in mice.4 Yet, the molecular process underlying Fn-dependent metastatic tumour formation was undefined. Earlier this year, three research groups, using a similar in vitro experimental design, reported that Fn infection enhanced migration of human CRC-derived HCT116 cells, although each group proposes distinct mechanisms.5–7 These include induction of interleukin-8 (IL-8) and C-X-C Motif Chemokine Ligand 1 (CXCL1),5 upregulation of …

Retracted: No

PubPeer comments:
 Several comments are available [here] . ,
MGC29506 induces cell cycle arrest and is downregulated in gastric cancer
Authors: ChangXin Shen
Yourong Fu
Li Tian
Ming Chen
Lin Xia
Journal: Cellular immunology (2013)
Discipline: IMMUNOLOGY
Keywords: PACAP; MGC29506; gene; cell cycle; apoptosis
Affiliations: Genetic Diagnosis Center, ZhongNan Hospital of Wuhan University, Wuhan 430071, China.

Abstract:  The proapoptotic caspase adaptor protein (PACAP) is involved in cell-cycle regulation and promotes apoptosis. Both MGC29506 and PACAP are isoforms of the MGC29506 gene and are generated by differential splicing of the alternative splice-acceptor. In studying PACAP, we inadvertently constructed the eukaryotic expression vector MGC29506. At present, the function of the MGC29506 gene is largely unknown with the key exception of information obtained by bioinformatics. We studied the role of MGC29506 in gastric cancer cell proliferation, the cell cycle and apoptosis. In addition, we studied MGC29506 expression in gastric cancer patients and explored its significance. We found that the expression of MGC29506 in gastric cancer samples was lower than in samples from adjacent non-tumor tissues. We found that the MGC29506 protein was localized in the cell nucleus of AGS cells and inhibited their proliferation. Higher percentages of G0/G1 and S phase cells were induced by transfection with the MGC29506 gene than were induced by transfection with the negative control. We showed that cells transfected with MGC29506 were arrested at the G0/G1 and S phases of the cell cycle. However, we found no significant increases in apoptosis of cells transfected with MGC29506 compared with cells transfected with the negative control. Our results suggested that MGC29506 has the potential of functioning as a novel suppressor gene in gastric cancer. Downregulation of MGC29506 may also promote the progression of gastric cancer. 

Retracted: No

PubPeer comments:
 Figure 2: In the images representing both of these conditions there appear very similar cells. Strangely, in the areas of the lower panels that appear similar, the green and blue channels do not appear to overlay in the way you would expect. ![file] In Figure 4, these FACS plots appear identical. The difference in the indicated percentages in each gate appear to be because the gates are placed in different positions. ![file] ,
Synthesis of silver nanoparticles using plant derived 4-N-methyl benzoic acid and evaluation of antimicrobial, antioxidant and antitumor activity
Authors: Sandhanasamy Devanesan
Mohamad S AlSalhi
P Murali
Kannan Elangovan
Amirtham Jacob A Ranjitsingh
Journal: Saudi Journal of Biological Sciences (2019)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Antibacterial; Antioxidant and antitumor; Bio inspired AgNPs; Memecylon.
Affiliations: Research Chair in Laser Diagnosis of Cancers, College of Science, Department of Physics and Astronomy, King Saud University, Riyadh 11451, Saudi Arabia., Department of Physics and Astronomy, College of Science, King Saud University, Riyadh 11451, Saudi Arabia., Green Signal Bio Pharma Private Limited, Pappankuppam Village, Tiruvallur District, Chennai 600025, Tamil Nadu, India., Department of Biotechnology, Prathyusha Engineering College, Chennai 602025, India.

Abstract:  The present study is to investigate the antitumor, antioxidant and antibacterial potential of silver nanoparticles (Ag NPs) synthesized from a phenolic derivative 4-N-methyl benzoic acid, isolated from a medicinal plant (Memecylon umbellatum Burm F). The Bio-inspired nanoparticles (NPs) were analyzed by using UV-vis spectroscopy, FTIR, HRTEM, Zeta potential and XRD techniques. The UV-vis spectroscopy study at the band of 430 nm confirmed the nanoparticles formation. HRTEM report showed that the AgNPs synthesized were in the size range 7-23 nm. The harvested nanoparticles were subjected to anti-bacterial assay and a dose dependent inhibitory action was observed against the tested human pathogens. Among the tested bacteria, Acinetobacter baumannii was found to be highly sensitive to AgNPs (diameter of zone of inhibition was 31 mm). Further, the silver nanoparticles exhibited a good anti-tumor activity against the breast cancer cell line (MCF 7) with an IC50 value of 42.19 µg/mL. As the present study confirmed a good antibacterial, antioxidant and antitumor activity in the nanoparticles synthesized using 4-N-methyl benzoic acid derived from a medicinal plant, the product can be further tested to formulate a good lead compound for biomedical applications. 

Retracted: No

PubPeer comments:
 image duplication ![file] Disclaimer: These potential image duplications have been detected automatically using ImageTwin http: dx.doi.org 10.1145 3019612.3019875 Although results have been curated, the automatic algorithm may have generated false positive results and cannot take into account all scientific explanations for apparent duplications like stripped and reprobed blots, time series, serial sections and reused controls. ,
Effect of SATB1 silencing on the proliferation, invasion and apoptosis of TE-1 esophageal cancer cells
Authors: Hongli Zhou
Bo Huang
Siwang Wang
Xiaodong Wang
Xianping Lang
Fei Xiong
Journal: Oncology letters (2017)
Discipline: CLINICAL MEDICINE
Keywords: TE-1; esophageal cancer; small interfering RNA; special AT-rich sequence-binding protein-1 gene.
Affiliations: Department of Thoracic Surgery, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121000, P.R. China., Department of Nephropathy, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121000, P.R. China.

Abstract:  The aim of the present study was to investigate the effect of special AT-rich sequence-binding protein-1 (SATB1)-targeted small interfering RNA (siRNA) on the proliferation, invasion and apoptosis of TE-1 human esophageal cancer cells. SATB1 has been correlated with the metastasis and poor prognosis of colon and breast cancer, but the role of SATB1 in esophageal cancer remains unknown. Therefore, the present study constructed and transfected SATB1-siRNA into TE-1 cells in order to knockdown the expression of the SATB1 gene. Western blot analysis, a cell counting kit, transwell chamber assays and flow cytometry were used to assess the effect of SATB1-siRNA on the proliferation, invasion and apoptosis of cells. The results demonstrated that the expression of the SATB1 gene was efficiently knocked down by SATB1-siRNA, and that SATB1-siRNA inhibited the proliferation, invasion and apoptosis of TE-1 cells. Therefore, it was concluded that the SATB1 gene is important in the pathogenesis of human esophageal cancer, and may present a novel therapeutic target for esophageal cancer. 

Retracted: No

PubPeer comments:
 Image concerns in this paper were found during a systematic search of papers in Spandidos journals for possible duplicated images. Figure 4. Three of the four panels appear to share similar groups of dots. Boxes of the same color highlight areas that look similar to each other. ![file] ,