PReD-Bench/PRed-Bench huggingface dataset:
Antioxidant treatment ameliorates germ cell apoptosis induced by a high-dose ionizing irradiation in rats
Authors: M Gorenberg
A G Coran
Y Pollak
O Nativ
Igor Sukhotnik
Y Ben-Shahar
I N Bejar
Journal: Pediatric Surgery International (2019)
Discipline: CLINICAL MEDICINE
Keywords: Antioxidant therapy; Apoptosis; Germ cell; Radiation; Rat.
Affiliations: Laboratory of intestinal adaptation and recovery, The Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel. ., Department of Pediatric Surgery, Bnai Zion Medical Center, 47 Golomb St., P.O.B. 4940, Haifa, 31048, Israel. ., Laboratory of intestinal adaptation and recovery, The Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel., Department of Pediatric Surgery, Bnai Zion Medical Center, 47 Golomb St., P.O.B. 4940, Haifa, 31048, Israel., Department of Urology, Bnai Zion Medical Center, Haifa, Israel., Section of Pediatric Surgery, C. S. Mott Children's Hospital, University of Michigan Medical School, Ann Arbor, Michigan, US., Department of Nuclear Medicine, Bnai Zion Medical Center, Haifa, Israel.

Abstract:  Background: Exposure to ionizing radiation results in cytotoxic and genotoxic effects caused mainly by the oxidative damage. In the present study, we investigated the radioprotective effect of novel antioxidant cocktail on germ cell apoptosis and spermatogenesis in rats subjected to whole body radiation (WBIR). Methods: Adult male rats weighing 250-270 g were divided into four groups, eight rats each. Group 1 served as untreated control, group 2 received an IP single dose of antioxidant cocktail (1 ml). Group 3 was exposed to a WBIR (6 Gy). Group 4 received antioxidant cocktail before WBIR. Rats from each group were killed after 48 h. MDA levels were measured in serum (TBARS assay). Johnsen's criteria and the number of germinal cell layers were used to categorize spermatogenesis. TUNEL assay was used to determine germ cell apoptosis. Statistical analysis was performed using one-way ANOVA test. Results: WBIR resulted in histological testicular damage (decrease in Johnsen's criteria, p &lt; 0.05) that was accompanied by a significant increase in germ cell apoptosis, expressed as the number of apoptotic cells per 100 tubules (AI-1 apoptotic index) and the number of positive tubules per 100 tubules (AI-2 apoptotic index). Treatment with antioxidant cocktail resulted in a significant decrease in germ cell apoptosis (33% decrease in AI-1, p &lt; 0.05 and 34% decrease in AI-2, p &lt; 0.05) that was accompanied by an improved spermatogenesis (increase in Johnsen's criteria, p &lt; 0.05). Conclusions: In a rat model of WBIR, antioxidant treatment ameliorates oxidative stress-induced testicular damage, decreases germ cell apoptosis and improves spermatogenesis. 

Retracted: No

PubPeer comments:
 Figure 3. * Blue boxes: The IR and IR-AOX panels appear to look more similar than expected. ![file] ,
Upregulation of microRNA-143-3p induces apoptosis and suppresses proliferation, invasion, and migration of papillary thyroid carcinoma cells by targeting MSI2
Authors: Cong Wang
Wei Liu
Zheng-Lin Wang
Zhi-Long Ai
Journal: Experimental and Molecular Pathology (2020)
Discipline: CLINICAL MEDICINE
Keywords: Invasion; Migration; Musashi RNA binding protein 2; Papillary thyroid carcinoma; Proliferation
Affiliations: Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, PR China., Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, PR China. Electronic address: .

Abstract:  As a tumor-associated biological molecule, microRNA-143-3p (miR-143-3p) is implicated in the progression of papillary thyroid carcinoma (PTC). We conducted this study to elucidate the effects of miR-143-3p mediated by Musashi RNA binding protein 2 (MSI2) on the biological activities of PTC cells. The K1 cells with the lowest miR-143-3p expression were selected for the experiments. The targeting relationship between miR-143-3p and MSI2 was verified. The biological functions of miR-143-3p and MSI2 with respect to K1 cell proliferation, cycle distribution, apoptosis, invasion, migration, and tumorigenesis were studied using gain- and loss-of-function assays both in vitro and in vivo. MSI2 was verified to be a target gene of miR-143-3p. Cells treated with upregulation of miR-143-3p or silencing of MSI2 exhibited significantly decreased the expression of Bcl-2, PCNA, MCM2, Ki67, MSI2, MMP-2, and MMP-9. This was accompanied by inhibited cell proliferation, cell invasion, and migration, as well as a significant increase in Bax expression, cell cycle arrest, and cell apoptosis. More importantly, the tumor inhibitory effects of upregulated miR-143-3p were also confirmed in the tumor xenografts in nude mice. Our results indicate that upregulation of miR-143-3p suppresses the progression of PTC by impeding cell growth, invasion, and migration via downregulation of MSI2, highlighting the potential of miR-143-3p as a target for future PTC treatment. 

Retracted: No

PubPeer comments:
 Fig 7C. ![file] Were these flow-cytometry cell-cycle plots hand-drawn? The G0 G1, S, and G2 M humps vary in *shape* (not just height) from panel to panel, which doesn t seem right. Each panel contains a wriggly line and a smoother line, where the former (I assume) is supposed to be the raw data and the latter is supposed to sum the G0 G1, S, and G2 M contributions -- except it doesn t. , 
  Acknowledgements We would like to thank our researchers for their hard work and reviewers for their valuable advice. I am puzzled. Are the authors thanking themselves? Or are they thanking some other people who **did the research** but do not warrant co-authorship or even acknowledgement by name? ,
Counter-regulatory effects of incremental hypoxia on the transcription of a cardiac fatty acid oxidation enzyme-encoding gene
Authors: Michael N Sack
Kholiswa C Ngumbela
M Faadiel Essop
Journal: Molecular and Cellular Biochemistry (2003)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Cardiac fatty acid oxidation; hypoxia; gene expression; metabolic switch; transcriptional control
Affiliations: Hatter Institute for Cardiology Research, University of Cape Town Medical School, Cape Town, South Africa.

Abstract:  Cardiac fatty acid oxidation (FAO) enzyme gene expression is known to be downregulated during hypoxia in concordance with reduced FAO rates. To evaluate this metabolic switch, the transcriptional control of a cardiac FAO enzyme-encoding gene (medium-chain acyl-CoA dehydrogenase, MCAD) was characterized in response to hypobaric hypoxia. Transgenic mice harboring 560-bp of the human MCAD gene promoter fused to the bacterial chloramphenicol acetyl transferase (CAT) reporter gene were exposed to moderate (14% O2) or severe (8% O2) hypoxia for 2 or 7 days. MCAD-CAT activity and gene expression were significantly downregulated following 7 days of moderate hypoxia versus normoxic controls (p &lt; 0.05). In parallel two known transcriptional regulators of MCAD expression, PPARalpha and Sp3, were concordantly downregulated at 7 days hypoxia. In contrast, severe hypoxia increased MCAD-CAT activity by 31 +/- 1.4% after 2 days hypoxia, returning to base +/- 4% after 2 days (p &lt; 0.001) and returned to control levels after 7 days of hypoxia. These data demonstrate that MCAD gene expression is downregulated after 7 days of moderate hypoxia and inversely regulated with severe hypoxia. The known MCAD transcriptional regulators PPARalpha and Sp3 mirror MCAD expression. These data indicate that the transcriptional regulatory circuits involved in the control of MCAD gene expression under hypoxic conditions are modulated by upstream factors that are sensitive to the levels of oxygen. 

Retracted: No

PubPeer comments:
 Figure 1B. * Red boxes: In the GAPDH panel, lanes 1-3 look similar to lanes 4-6. Figure 3C. * Blue boxes: In the GAPDH panel, lanes 1-3 look similar to lanes 4-6. Reported to the journal in October 2015, with a friendly reminder in 2017, but no response as of today. I would love to hear from the authors if the journal ever contacted them in the past five years. ![file] ,
Functional selection of protease inhibitory antibodies
Authors: Aaron Ramirez
Ki Baek Lee
Chuan Chen
Ru-Rong Ji
Xin Ge
Xin Luo
Tyler Lopez
Zahid Mustafa
Chris Benitez
Journal: Proceedings of the National Academy of Sciences of the United States of America (2019)
Discipline: Multidisciplinary
Keywords: BACE-1; MMP; functional selection; monoclonal antibody; protease inhibitor.
Affiliations: Department of Chemical and Environmental Engineering, University of California, Riverside, CA 92521., Center for Translational Pain Medicine, Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710., Department of Chemical and Environmental Engineering, University of California, Riverside, CA 92521; .

Abstract:  Critical for diverse biological processes, proteases represent one of the largest families of pharmaceutical targets. To inhibit pathogenic proteases with desired selectivity, monoclonal antibodies (mAbs) hold great promise as research tools and therapeutic agents. However, identification of mAbs with inhibitory functions is challenging because current antibody discovery methods rely on binding rather than inhibition. This study developed a highly efficient selection method for protease inhibitory mAbs by coexpressing 3 recombinant proteins in the periplasmic space of Escherichia coli-an antibody clone, a protease of interest, and a β-lactamase modified by insertion of a protease cleavable peptide sequence. During functional selection, inhibitory antibodies prevent the protease from cleaving the modified β-lactamase, thereby allowing the cell to survive in the presence of ampicillin. Using this method to select from synthetic human antibody libraries, we isolated panels of mAbs inhibiting 5 targets of 4 main protease classes: matrix metalloproteinases (MMP-14, a predominant target in metastasis; MMP-9, in neuropathic pain), β-secretase 1 (BACE-1, an aspartic protease in Alzheimer's disease), cathepsin B (a cysteine protease in cancer), and Alp2 (a serine protease in aspergillosis). Notably, 37 of 41 identified binders were inhibitory. Isolated mAb inhibitors exhibited nanomolar potency, exclusive selectivity, excellent proteolytic stability, and desired biological functions. Particularly, anti-Alp2 Fab A4A1 had a binding affinity of 11 nM and inhibition potency of 14 nM, anti-BACE1 IgG B2B2 reduced amyloid beta (Aβ40) production by 80% in cellular assays, and IgG L13 inhibited MMP-9 but not MMP-2/-12/-14 and significantly relieved neuropathic pain development in mice. 

Retracted: No

PubPeer comments:
 In 2021, there was published an attempted (failed) replication of this study (plus an additional, relevant study) - published as a Registered Report: Motes-Rodrigo, A., Mundry, R., Call, J., Tennie, C. (2021). Evaluating the influence of action-and subject-specific factors on chimpanzee action copying. Royal Society Open Science, 8(2), 200228. available here: https: doi.org 10.1098 rsos.200228 ,
An atypical tumor necrosis factor (TNF) receptor-associated factor-binding motif of B cell-activating factor belonging to the TNF family (BAFF) receptor mediates induction of the noncanonical NF-kappaB signaling pathway
Authors: Minying Zhang
William Reiley
Matthew D Morrison
Shao-Cong Sun
Journal: Journal of Biological Chemistry (2005)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: BAFF receptor; TNF receptor superfamily; B cells; NF-kappaB; signaling pathway
Affiliations: Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, 500 University Dr., Hershey, Pennsylvania 17033, USA.

Abstract:  BAFF receptor (BAFFR) is a member of the TNF receptor (TNFR) superfamily that regulates the survival and maturation of B cells. BAFFR exerts its signaling function by inducing activation of NF-kappaB, although the underlying mechanism has not been well defined. By using a chimeric BAFFR, we show that BAFFR preferentially induces the noncanonical NF-kappaB signaling pathway. This specific function of BAFFR is mediated by a sequence motif, PVPAT, which is homologous to the TRAF-binding site (PVQET) present in CD40, a TNFR known to induce both the canonical and noncanonical NF-kappaB pathways. Mutation of this putative TRAF-binding motif within BAFFR abolishes its interaction with TRAF3 as well as its ability to induce noncanonical NF-kappaB. Interestingly, modification of the PVPAT sequence to the typical TRAF-binding sequence, PVQET, is sufficient to render the BAFFR capable of inducing strong canonical NF-kappaB signaling. Further, this functional acquisition of the modified BAFFR is associated with its stronger and more rapid association with TRAF3. These findings suggest that the PVPAT sequence of BAFFR not only functions as a key signaling motif of BAFFR but also determines its signaling specificity in the induction of the noncanonical NF-kappaB pathway. 

Retracted: No

PubPeer comments:
 Figure 1C. https: imgur.com 9ujNI7E , 
 Figure 4A. Much more similar than expected. https: imgur.com GecA5op ,
Nm23-H1 can induce cell cycle arrest and apoptosis in B cells
Authors: Pankaj Kumar
Sushil K Sahu
Suchitra Mohanty
Tathagata Choudhuri
Subhash C Verma
Masanao Murakami
Erle S Robertson
Rajeev Kaul
Journal: Cancer biology & therapy (2010)
Discipline: CLINICAL MEDICINE
Keywords: Nm23-H1; tumor metastasis suppressor; nucleoside-diphosphate kinase; cellular activities; signaling pathway
Affiliations: Division of Infectious Disease Biology, Institute of Life Sciences, Bhubaneswar, India.

Abstract:  Nm23-H1 is a well-known tumor metastasis suppressor, which functions as a nucleoside-diphosphate kinase converting nucleoside diphosphates to nucleoside triphosphates with an expense of ATP. It regulates a variety of cellular activities, including proliferation, development, migration and differentiation known to be modulated by a series of complex signaling pathway. Few studies have addressed the mechanistic action of Nm23-H1 in the context of these cellular processes. To determine the downstream pathways modulated by Nm23-H1, we expressed Nm23-H1 in a Burkitt lymphoma derived B-cell line BJAB and performed pathway specific microarray analysis. The genes with significant changes in expression patterns were clustered in groups which are responsible for regulating cell cycle, p53 activities and apoptosis. We found a general reduction of cell cycle regulatory proteins including cyclins and cyclin dependent kinase inhibitors (anti proliferation), and upregulation of apoptotic genes which included caspase 3, 9 and Bcl-x. Nm23-H1 was also found to upregulate p53 and downregulate p21 expression. A number of these genes were validated by real time PCR and results from promoter assays indicated that Nm23-H1 expression downregulated cyclin D1 in a dose responsive manner. Further, we show that Nm23-H1 forms a complex with the cellular transcription factor AP1 to modulate cyclin D1 expression levels. BJAB cells expressing Nm23-H1 showed reduced proliferation rate and were susceptible to increased apoptosis which may in part be due to a direct interaction between Nm23-H1 and p53. These results suggest that Nm23-H1 may have a role in the regulation of cell cycle and apoptosis in human B-cells. 

Retracted: No

PubPeer comments:
 Figure 3. Much more similar than you would expect. https: imgur.com QifpE1c , 
 Figure 7A. Much more similar than you would expect. https: imgur.com bVQJpKf , 
 Figure 7B. Much more similar than you would expect. https: imgur.com cq2ntoP , 
 Well spotted, Paspalum Laeve. An additional finding in Figure 3: Lane 6 appears to look very similar to lanes 5, 7, and 10 as well, albeit stretched a bit. Quite a bit, actually. ![file]  This work was supported by NIH grants NCI CA72150-07, NCI CA91792-01, NIDCR DE14136-01 and NCI CA108461 to E.S.R. E.S.R. is a scholar of the Leukemia and Lymphoma Society of America. Also partially supported by Institute of Life Sciences (Dept of Biotechnology, India) core grant. ,
The effect of autophagy and mitochondrial fission on Harderian gland is greater than apoptosis in male hamsters during different photoperiods
Authors: Lai-Xiang Xu
Jin-Hui Xu
Lei Chen
Xiao-Cui Geng
Xiang-Yu Zhao
Ming Wu
Jun-Jie Mou
Hui-Liang Xue
Zhe Wang
Journal: PLoS ONE (2020)
Discipline: Multidisciplinary
Keywords: Photoperiod; Harderian gland; Melatonin; HIOMT; Autophagy
Affiliations: College of Life Sciences, Qufu Normal University, Qufu, Shandong, China., Yiheyuan School, Yiyuan, Shandong, China.

Abstract:  Photoperiod is an important factor of mammalian seasonal rhythm. Here, we studied morphological differences in the Harderian gland (HG), a vital photosensitive organ, in male striped dwarf hamsters (Cricetulus barabensis) under different photoperiods (short photoperiod, SP; moderate photoperiod, MP; long photoperiod, LP), and investigated the underlying molecular mechanisms related to these morphological differences. Results showed that carcass weight and HG weight were lower under SP and LP conditions. There was an inverse correlation between blood melatonin levels and photoperiod in the order SP &gt; MP &gt; LP. Protein expression of hydroxyindole-O-methyltransferase (HIOMT), a MT synthesis-related enzyme, was highest in the SP group. Protein expression of bax/bcl2 showed no significant differences, indicating that the level of apoptosis remained stable. Protein expression of LC3II/LC3I was higher in the SP group than that in the MP group. Furthermore, comparison of changes in the HG ultrastructure demonstrated autolysosome formation in the LP, suggesting the lowest autophagy level in under MP. Furthermore, the protein expression levels of ATP synthase and mitochondrial fission factor were highest in the MP group, whereas citrate synthase, dynamin-related protein1, and fission1 remained unchanged in the three groups. The change trends of ATP synthase and citrate synthase activity were similar to that of protein expression among the three groups. In summary, the up-regulation of autophagy under SP and LP may be a primary factor leading to loss of HG weight and reduced mitochondrial energy supply capacity. 

Retracted: No

PubPeer comments:
 In Figure 3, a micrograph has been duplicated and presented as something else. ![file] ,
Retracted : Prognostic significance of long non‐coding RNA MALAT1 for predicting the recurrence and metastasis of gallbladder cancer and its effect on cell proliferation, migration, invasion, and apoptosis
Authors: Ke-Ke Sun
Ping-Ping Hu
Feng Xu
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MALAT1; apoptosis; gallbladder cancer; invasion; metastasis
Affiliations: Department of GastroenterologyYinzhou Hospital Affiliated to Medical School of Ningbo University (Yinzhou People's Hospital)NingboChina

Abstract:  The objective of this study is to explore the role of MALAT1 as a molecular indicator in predicting the recurrence, metastasis, and prognosis of gallbladder cancer (GBC) and its effect on the proliferation, invasion, migration, and apoptosis of GBC cells in vitro. GBC tissues and adjacent normal tissues were collected from 102 patients. MALAT1 short hairpin RNA (shRNA) plasmids were first constructed to transfect the GBC-SD cells. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was applied to detect MALAT1 expression. CCK-8 assay, flow cytometry, and Transwell assay were applied to testify the cell proliferation, cell cycle, apoptosis, invasion, and migration. A receiver operating characteristic (ROC) curve was used to evaluate the values of MALAT1 in GBC recurrence, metastasis, and prognosis. COX regression analysis was applied to analyze the independent influencing factors of GBC patients' survival status. ROC curve results showed that the MALAT1 expression could be a predictor of the GBC recurrence, metastasis, and prognosis. According to the COX regression analysis, MALAT1 expression, tumor size, and TNM stage were independent influencing factors of GBC patients' survival condition. Compared with the GBC-SD cells transfected with empty plasmids, those transfected with MALAT1 shRNA plasmids showed higher apoptosis rates, weakened proliferation, migration, and invasion. In conclusion, our findings demonstrate that lncRNA MALAT1 can be considered as an indicator for evaluating the recurrence, metastasis, and prognosis of GBC patients. We also demonstrate how the overexpression of MALAT1 confers an oncogenic function in GBC. 

Retracted: Yes

PubPeer comments:
 The same or similar cells seem to appear multiple times in images in figure 5A. ![file] , 
 #1 ![file] Here color-coded to draw attention to similar panels in Fig 10B of [He et al (2018)] , ![] and Fig 11 A,B of [Liao et al (2018)] . ![] , 
 Retracted [30 June 2021] . ------------------------- The above article, published online on 23 October 2017 in Wiley Online Library has been retracted by agreement between the the journal s Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. As several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. ,
RETRACTED ARTICLE: EpCAM: A Potential Antimetastatic Target for Gastric Cancer
Authors: Jie Liu
Hongzan Ji
Daiming Fan
Li Wang
Wenqi Du
Feihu Bai
Shanshan Cao
Journal: Digestive Diseases and Sciences (2010)
Discipline: CLINICAL MEDICINE
Keywords: Epithelial cellular adhesion molecule (EpCAM); immunotherapeutic target; metastasis; Edrecolomab; monoclonal antibody
Affiliations: State Key Laboratory of Cancer Biology, Digestive Diseases of Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi Province, People's Republic of China.

Abstract:  Purpose: Epithelial cellular adhesion molecule (EpCAM) is an attractive immunotherapeutic target to overcome metastasis of a variety of epithelium-oriented cancers. Edrecolomab, one kind of EpCAM monoclonal antibody (Panorex), has been approved for clinical application as postoperative adjuvant therapy in breast and colorectal cancer. However, the role of EpCAM in gastric cancer metastasis remains unclear. Results: EpCAM was found to be more highly overexpressed in metastatic gastric cancer than in nonmetastatic samples by immunohistochemistry staining. The expression level of EpCAM in gastric cancer cell lines was determined by reverse-transcription polymerase chain reaction (RT-PCR) and Western blotting, respectively. Downregulation of EpCAM by small interfering RNA (siRNA) significantly suppressed in vitro adhesive, invasive, and migratory and in vivo metastatic abilities of gastric cancer cells. Conclusion: We provide first evidence that EpCAM contributes to the migration of gastric cancer, suggesting that EpCAM-targeted therapy might be a promising strategy in metastatic gastric cancer. 

Retracted: Yes

PubPeer comments:
 Retraction note: EpCAM: a potential antimetastatic target for gastric cancer EpCAM: A Potential Antimetastatic Target for Gastric Cancer by Wenqi Du, Hongzan Ji, Shanshan Cao, Li Wang, Feihu Bai, Jie Liu, Daiming Fan published online in Digestive Diseases and Sciences on November 26, 2009, DOI 10.1007 s10620-009-1033-8 is retracted as the article plagiarized the content from the following article: EpCAM is overexpressed in gastric cancer and its downregulation suppresses proliferation of gastric cancer by Du Wenqi, Wang Li, Cao Shanshan, Chen Bei, Zhang Yafei, Bai Feihu, Liu Jie, Fan Daiming published online on March 18, 2009, by Journal of Cancer Research and Clinical Oncology, DOI 10.1007 s00432-009-0569-5. ,
CXCR6 predicts poor prognosis in gastric cancer and promotes tumor metastasis through epithelial-mesenchymal transition
Authors: Zi-Wen Long
Qiong-Zhu Dong
Xiao-Wen Liu
Hua Huang
Ya-Nong Wang
Jie-Jie Jin
Qi Hong
Ye Zhou
Hong Cai
Fa-Xiang Dai
Journal: Oncology Reports (2017)
Discipline: CLINICAL MEDICINE
Keywords: Chemokines; CXCL16; CXCR6; Gastric cancer; Metastasis
Affiliations: Gastric Surgery Department, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China., Department of Hepatobiliary Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, P.R. China., Institutes of Biomedical Science, Fudan University, Shanghai 200032, P.R. China.

Abstract:  Chemokines and their receptors have been confirmed to be involved in several types of cancer. However, little is known concerning the role of CXCL16 and its receptor CXCR6 in gastric cancer (GC) progression and metastasis. In the present study, expression of CXCL16 and CXCR6 in GC tumor and peritumoral tissues was detected by immunohistochemistry (IHC) in a cohort of 352 GC patients who underwent gastrectomy, and the correlation between CXCL16/CXCR6 expression and clinicopathological characteristics was further analyzed. To evaluate the function of CXCR6, we overexpressed and knocked down CXCR6 in GC cell lines. Results showed that expression of CXCR6, but not CXCL16, was significantly upregulated in GC tumor tissues, and was significantly correlated with lymph node and distant metastases, and advanced clinical stage in the GC patients. Survival analysis showed that large tumor size (&gt;5 cm), elevated preoperative serum carcinoembryonic antigen (CEA) level, advanced TNM stage and high CXCR6 expression indicated worse overall survival (OS) and disease-free survival (DFS) in GC, and CXCR6 was an independent predictor for both OS and DFS in GC. In vitro experiments showed that CXCR6 overexpression induced cell migration and invasion ability, and promoted epithelial-mesenchymal transition of GC cells by upregulation of mesenchymal markers and inhibition of epithelial markers. In contrast, knockdown of CXCR6 in GC cells resulted in inhibition of cell proliferation, migration and invasion ability, and reversal of epithelial-mesenchymal transition (EMT) phenomenon. Our results demonstrated that CXCR6 is an independent prognostic factor for poor survival in GC patients, and may promote GC metastasis through EMT. 

Retracted: No

PubPeer comments:
 Fig 3C Potential overlap between images of migration of WT and Ctrl ![file] , 
 Fig 4A Invasion of WT and migration of CXCR6-sh might be more similar than expected. ![file] ,
Therapeutic effect of Colla corii asini on improving anemia and hemoglobin compositions in pregnant women with thalassemia
Authors: Yanfang Li
Daocheng Li
Xiangyi Li
Lilin Yang
Hui He
Songping Luo
Journal: International journal of hematology (2016)
Discipline: CLINICAL MEDICINE
Keywords: Anemia; Colla corii asini; Hemoglobin; Pregnancy; Thalassemia.
Affiliations: Department of Obstetrics, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China., Department of Clinical Laboratory, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China., First School of Clinical Medicine, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, China., First School of Clinical Medicine, Guangzhou University of Chinese Medicine, No. 12 Jichang Road, Guangzhou, 510405, Guangdong, China. .

Abstract:  Currently there is no consensus on treating anemia in pregnant thalassemia patients. In China, Colla corii asini (CCA) has been widely used for treating anemia for more than 2000 years. However, its clinical application in the thalassemia population is limited by a lack of quantitative evidence. The present study aims to investigate the therapeutic effect of CCA in increasing hemoglobin (Hb) concentration and improving abnormal hemoglobin compositions in pregnant patients with β-thalassemia. Seventy-two pregnant patients who met inclusion criteria were randomly assigned to either the treatment group or control group. Patients in the treatment group were given 15 g of CCA, while the control group were observed and followed up without any treatment. Levels of Hb, serum iron (SI), serum ferritin (SF) and three types of Hb components [adult hemoglobin (HbA), fetal hemoglobin (HbF), minor adult hemoglobin (HbA2)] were measured before and after treatment. Treatment with CCA led to a significant increase of Hb. The major Hb component induced by CCA was HbA, while levels of both HbA2 and HbF dropped after treatment. CCA treatment significantly increased SI, while SF remained unaffected. Our data suggest that CCA can improve anemia and optimize Hb components in pregnant patients with thalassemia without affecting iron reserves. 

Retracted: No

PubPeer comments:
 I have the following two concerns: 1. The statistics performed by the authors are not persuasive. In table 2 the authors tested the significant difference of u2206Hb between Treatment group and control group. What is the rationale of doing that? Usually, we should independently test the significant difference of Hb level within the treatment group beforehand and afterward, as well as the control group. 2. The authors declared that u201cPatients in control groups do not receive any intervention.u201d But I think a placebo-treatment is necessary. ,
miR-21, miR-17 and miR-19a induced by phosphatase of regenerating liver-3 promote the proliferation and metastasis of colon cancer
Authors: D Lai
S Chen
H Ye
C He
Z Xiao
J Wang
Z Chu
J Zhang
J Sun
Journal: British Journal of Cancer (2012)
Discipline: CLINICAL MEDICINE
Keywords: Phosphatase of regenerating liver-3 (PRL-3); miR-21; miR-17; miR-19a; colorectal cancer (CRC)
Affiliations: Department of Hepatobiliary Surgery, Sun-Yat-Sen Memorial Hospital, Sun-Yat-Sen University, 107 Yanjiang West Road, Guangzhou 510120, China.

Abstract:  Background: Phosphatase of regenerating liver-3 (PRL-3) is an oncogene known to promote tumour metastasis, especially in colorectal cancer (CRC). Here, we demonstrate that the miR-21, miR-17 and miR-19a expressions induced by PRL-3 are involved in the proliferation and metastasis of colon cancer. Methods: Microarray analysis and quantitative reverse-transcription polymerase chain reactions (qRT-PCR) were used to investigate the changes in miRNA expression due to the overexpression of PRL-3. Transwell chamber invasion assays, CCK-8 proliferation assays and RNA interference assays were used to explore the effects of PRL-3 on miR-21, miR-17 and miR-19a expression in colon cancer cells. Immunohistochemistry and qRT-PCR were performed in colon cancer tissues to evaluate the expression of PRL-3, signal transducer and activator of transcription 3 (STAT3), miR-21, miR-17 and miR-19a. Results: Our study demonstrated that the overexpression of PRL-3 in colon cancer cells induced the expression of miR-21, miR-17 and miR-19a by activating STAT3. Subsequently, these microRNAs contributed to the increased proliferation and invasiveness of the colon cancer cells. Positive correlations between PRL-3 and these microRNAs were also observed in matched primary colon cancer tissues and metastatic lesions. Conclusion: miR-21, miR-17 and miR-19a induced by PRL-3 contribute to the proliferation and invasion of colon cancer. 

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. ,
In vivo host interactions with mineral trioxide aggregate and calcium hydroxide: inflammatory molecular signaling assessment
Authors: Claudia P Figueiredo
Mabel M Cordeiro
Mara S Felippe
Adair R S Santos
Wilson T Felippe
Jessie F Reyes-Carmona
Journal: Journal of Endodontics (2011)
Discipline: CLINICAL MEDICINE
Keywords: Mineral trioxide aggregate; calcium hydroxide; dentinogenesis; cementogenesis; inflammatory signaling molecules
Affiliations: Postgraduate Dentistry Program of the Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil. 

Abstract:  Introduction: Mineral trioxide aggregate (MTA) and calcium hydroxide [Ca(OH)(2)] are promising biomaterials for stimulating dentinogenesis and cementogenesis. This research was undertaken to understand how MTA and CA(OH)(2) participate in the inflammatory, healing, and biomineralization processes. In this part of the study, we evaluated inflammatory signaling molecules promoted by in vivo host interaction with MTA and Ca(OH)(2). Methods: Human dentin tubes were filled with ProRoot MTA (Dentsply Tulsa Dental, Tulsa, OK), Ca(OH)(2), or kept empty. After 12 hours and 1, 3, 7, 15, 30, and 60 days of implantation in subcutaneous tissues in the backs of mice, the tubes and surrounding tissues were retrieved for cytokine level quantification and histological and immunohistochemical analysis. Results: MTA and Ca(OH)(2) induced proinflammatory cytokine up-regulation for up to 3 days. Moreover, interleukin-10 overexpression was noted on the tissue in contact with the biomaterials during the acute phase of the inflammatory reaction. Immunohistochemical analyses showed an increased expression of myeloperoxidase, nuclear factor kappa B (NF-κB), cyclooxygenase-2, inducible nitric oxide synthase enzymes, and vascular endothelial growth factor on day 1 for all groups. Conclusions: MTA and Ca(OH)(2) increased the activation of the NF-κB signaling system on day 1 for all groups. This finding can be associated with a proinflammatory and pro-wound healing environment, which was promoted earlier by MTA. 

Retracted: No

PubPeer comments:
 Figure 2: It seems that there s an overlap between the figures. Could authors check and provide an explanation, please? ![file] Figure 7: More similar than expected ![file] ,
Shufengjiedu capsules protect against neuronal loss in olfactory epithelium and lung injury by enhancing autophagy in rats with allergic rhinitis
Authors: Zhentao Zhao
Jinyu Mei
Yatang Wang
Ziyu Chen
Jianming Yang
Hua Kong
Journal: Bioscience trends (2020)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: Shufengjiedu capsules; allergic rhinitis; apoptosis; autophagy; inflammation.
Affiliations: Department of Otorhinolaryngology Head and Neck Surgery, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China., Department of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China., The Second Clinical College of Medicine, Anhui Medical University, Hefei, Anhui, China.

Abstract:  Shufengjiedu capsules (SFJDCs), a traditional Chinese medicine, have been widely used as an antiviral, antibacterial, antitumor, and anti-inflammatory drug. However, the roles of SFJDCs in allergic rhinitis remain unclear. The purpose of this study was to investigate the effects of SFJDCs in olfaction and lung injury in rats with allergic rhinitis. An animal model of allergic rhinitis was created by intraperitoneal injection and intranasal administration of ovalbumin to rats. All rats were divided into seven groups: a model group, a low-dose SFJDC group, a medium-dose SFJDC group, a high-dose SFJDC group, a cetirizine group, and a control group. Hematoxylin and eosin (HE) staining was used to observe pathological changes in rat lung and olfactory epithelium (OE) tissue, and peripheral blood was collected and subjected to an enzyme-linked immunosorbent assay (ELISA) to detect IgE, tumor necrosis factor alpha (TNF-α), and IL-1ꞵ levels. Western blotting, immunohistochemistry staining, and immunofluorescence staining were performed to detect inflammatory cytokines and levels of the autophagy biomarker beclin1 and the apoptosis biomarker cleaeved-caspased3 in lung and OE tissue. ELISA indicated that SFJDCs significantly decreased IgE, TNF-α, and IL-1ꞵ levels in peripheral blood, the lungs, and OE tissue. In addition, Western blotting and staining indicated that SFJDCs repair lung injury, protect against neuronal apoptosis in OE, and rescue impaired autophagy in the lungs and OE tissue. In conclusion, results indicated that SFJDCs might protect against neuronal loss in the OE and lung injury by enhancing autophagy and decreasing apoptosis in rats with allergic rhinitis. Therefore, SFJDCs might serve as an alternative treatment for allergic rhinitis. 

Retracted: No

PubPeer comments:
 Figure 1D appears to include a repeated image. *** ![file] , 
 #1 #1 We misplaced the picture of cetirizine group in Figure1D. We are very sorry for our mistake and carelessness. We will contact the BST editor to correct this mistake. Thank you for your comments. , 
 #1 We misplaced the picture of cetirizine group in Figure1D. We are very sorry for our mistake and carelessness. We will contact the BST editor to correct this mistake. Thank you for your comments. ,
MiRNA-1179 suppresses the metastasis of hepatocellular carcinoma by interacting with ZEB2
Authors: F-Z Gao
X-F Chen
H-B Gao
Journal: European review for medical and pharmacological sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: miRNA-1179; hepatocellular carcinoma; ZEB2; metastasis; prognosis
Affiliations: Department of Infectious Diseases, Binzhou People's Hospital, Binzhou, China. .

Abstract:  Objective: To investigate the biological function of microRNA-1179 (miRNA-1179) in regulating the proliferative and migratory abilities of the hepatocellular carcinoma (HCC) by targeting zinc-finger E-box-binding homeobox 2 (ZEB2). Patients and methods: The miRNA-1179 level in 40 HCC tissues and matched normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The association between the miRNA-1179 level and the clinical parameters of HCC patients was analyzed. The regulatory effects of miRNA-1179 on influencing proliferative and migratory abilities of HepG2 and Bel-7402 cells were assessed. The dual-luciferase reporter gene assay was conducted to verify the binding relationship between miRNA-1179 and ZEB2. Subsequently, the expression pattern and the biological function of ZEB2 in HCC were explored. The rescue experiments were finally carried out to uncover the role of the miRNA-1179/ZEB2 axis in regulating the progression of HCC. Results: MiRNA-1179 was downregulated in HCC tissues and cell lines. HCC patients with low expression of miRNA-1179 had higher metastatic rates (lymphatic metastasis and distant metastasis) and worse prognosis relative to those with low expression. The overexpression of miRNA-1179 attenuated the proliferative and migratory abilities of HCC cells. ZEB2 was confirmed to be the direct target of miRNA-1179 and its level was negatively regulated by miRNA-1179. ZEB2 was upregulated in HCC tissues and cell lines. The high expression of ZEB2 predicted a worse prognosis of HCC. The overexpression of ZEB2 reversed the inhibitory effects of miRNA-1179 on the proliferative and migratory abilities in HCC cells. Conclusions: MiRNA-1179 is closely related to lymphatic metastasis, distant metastasis, and overall survival of HCC. It alleviates the malignant progression of HCC by downregulating ZEB2. 

Retracted: No

PubPeer comments:
 Fig 4C.  A negative correlation between the expression levels of miR-1179 and ZEB2 in HCC tissues. D, The Kaplan-Meier curves revealed the overall survival in HCC patients with high and low expression of ZEB2. Rescaled for comparison with (right) a superimposition of 20 versions of the same scatterplot, from 20 papers from a papermill. Darker data-points appear in more of the variants. ![file] , 
 Another recurring feature of the products of this papermill are pairs of Kaplan-Meier plots resembling walls of Lego, where survival drops precipitously at 75 months after patient recruitment. Here, Figs 1D and 4D.  The Kaplan-Meier curves revealed the overall survival in HCC patients with high and low expression of miR-1179 ...  The Kaplan-Meier curves revealed the overall survival in HCC patients with high and low expression of ZEB2 . ![file] ,
Association between EGFR mutation and expression of BRCA1 and RAP80 in non-small cell lung cancer
Authors: Ming Yuan
Nanyao Wang
Dan Wu
Huafang Yin
Qiong Wang
Yanhua Fei
Fangbo Cui
Xia Sun
Journal: Oncology letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: BRCA1; EGFR mutation; RAP80; non-small cell lung cancer.
Affiliations: Department of Oncology, The Affiliated Jiangyin Hospital of Southeast University Medical College, Wuxi, Jiangsu 214400, P.R. China., Department of Oncology, The People's Hospital of Ma'Anshan, Maanshan Shi, Anhui 243000, P.R. China.

Abstract:  Association between the epithelial growth factor receptor (EGFR) mutation and the expression of breast cancer 1 (BRCA1) and receptor-associated protein 80 (RAP80) in non-small cell lung cancer (NSCLC) was studied. From September 2014 to September 2016, 51 patients with NSCLC who were hospitalized in Department of Thoracic Surgery in The Affiliated Jiangyin Hospital of Southeast University Medical College and underwent biopsy or operation were selected. The pathological changes of lung tissue were detected by hematoxylin and eosin histopathological staining. The fluorescent expression of BRCA1 and RAP80 protein in the two groups was determined by immunofluorescence staining. Reverse transcriptase polymerase chain reaction method and western blot analysis were used to detect BRCA1 and RAP80 mRNA and protein expression. Then the EGFR gene mutation was detected and analyzed. The results show that non-small cell lung cancer has an association with smoking. Compared with the control, the lung tissue structure of the NSCLC group was damaged. The protein fluorescence expression of BRCA1 and RAP80 in non-small cell lung cancer group was significantly increased. The expression of BRCA1 and RAP80 mRNA and protein in NSCLC group was significantly increased. The difference in expression of BRCA1 and RAP80 in the control and the non-small cell lung cancer group was statistically significant (P&lt;0.05). EGFR gene mutations detected 14 of the 51 patients with genetic mutations. Non-small cell lung cancer and smoking have certain relevance, and BRCA1 and RAP80 expression in the development and progression of NSCLC has a close relationship. EGFR mutation in non-small cell lung cancer significantly related to the mutation of EGFR and BRCA1 and RAP80 gene expression plays an important role in the diagnosis and treatment of NSCLC. 

Retracted: No

PubPeer comments:
 Figure 3C, the 24 and 48 FACS plot are duplicated ![file] , 
 #1 Thank you very much for finding out this comment. Due to our drawing errors, the 24 and 48 FACS plot are actually duplicated. We will correct this error according to our primary data through editor. , 
 **CORRECTION** published: https: translational-medicine.biomedcentral.com articles 10.1186 s12967-021-02917-z , 
 thanks for your valuable information correcting our error. ,
MicroRNA‑146a‑5p enhances ginsenoside Rh2‑induced anti‑proliferation and the apoptosis of the human liver cancer cell line HepG2
Authors: Yurong Qiu
Weiwen Chen
Haixia Li
Shuai Chu
Journal: Oncology Letters (2018)
Discipline: CLINICAL MEDICINE
Keywords: antitumor; ginsenoside Rh2; liver cancer; microRNA-146a-5p; promotion.
Affiliations: Medical Laboratories, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China., Medical Laboratories, Guangzhou Twelfth People's Hospital, Guangzhou, Guangdong 510620, P.R. China.

Abstract:  Liver cancer is one of the leading causes of malignancy-associated mortality worldwide and its clinical therapy remains very challenging. Ginsenoside Rh2 (Rh2) has been reported to have antitumor effects on some types of cancer, including liver cancer. However, its regulatory mechanism has not been extensively evaluated. In the present study, Rh2 increased the expression of microRNA (miR)-200b-5p, miR-224-3p and miR-146a-5p, and decreased the expression of miR-26b-3p and miR-29a-5p. Of the three upregulated miRs, miR-146a-5p exhibited the highest fold elevation. In accordance with a previous study, Rh2 effectively inhibited the survival of liver cancer cells in vitro and in a mouse model. In addition, it was observed that Rh2 markedly promoted liver cancer apoptosis and inhibited colony formation. Cell apoptosis and the inhibition of cell survival as well as colony formation induced by Rh2 were enhanced and weakened by miR-146a-5p overexpression and inhibition, respectively. The results of the present study provide further evidence of the antitumor effect of Rh2 in liver cancer and also demonstrate that this effect may be mediated via the regulation of miR-146a-5p expression in the liver cancer cell line HepG2. The results indicated that miR-146a-5p may be a promising regulatory factor in Rh2-mediated effects in liver cancer. 

Retracted: No

PubPeer comments:
 Fig 3C.  Results of western blot analysis indicate that miR-150 attenuates the NF-u03baB signaling pathway and then phosphorylation of P50 and P65 by negatively targeting PTX3 (n = 3). Panel C, protein bands of pentraxin-3, p-P50, and p-P65 in mouse coronary arteries . ![file] The control band, and two protein blobs in particular, manifests many times in otherwise-unrelated papers. For instance, Fig 9A from [Wu et al (2018a)] , or 5C of [Wu et al (2018b)] . ![] Fig 5A of [Ma et al (2019)] : ![] 5B of [Yan et al (2019)] : ![] Other examples in linked threads. , 
 Fig 3D.  protein bands of pentraxin-3, p-P50, and p-P65 B in endothelial cells . ![file] The loading control appears to be the same as the one seen in 7C of [Lu et al (2018)] and 6C of [Jiang et al (2018)] ... ![] ...or Fig 8A of [Wu et al (2018)] , though there identified as beta-Actin rather than as GAPDH. ![] Other examples in the linked threads. ,
TPD52L2 impacts proliferation, invasiveness and apoptosis of glioblastoma cells via modulation of wnt/β-catenin/snail signaling
Authors: Chen Lei
Lu Yun-Tao
Annie Huang
Xiang Wei
Li Jun-Jie
Zhou Qiang
Qi Song-Tao
Liu Ya-Wei
Li Hong
Wang Hai
Lei Bing-Xi
Journal: Carcinogenesis (2018)
Discipline: CLINICAL MEDICINE
Keywords: Intratumoral heterogeneity; target therapy; glioblastoma; GBM cells; biological phenotypes
Affiliations: Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China., Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China, Brain Tumor Research Center, Hospital for Sickkids, Toronto, Canada.

Abstract:  Intratumoral heterogeneity greatly hinders efficiency of target therapy in glioblastoma (GBM). To decipher the underlying mechanisms of heterogeneity, patient-derived adult GBM cells were separately isolated from margins of T1 gadolinium enhancing tumor lesions (PNCs) and T1 gadolinium enhancing core lesions (ECs). Single clone culture was conducted in ECs and U87MG cell line to screen clones with distinct biological phenotypes. Single cell clones with diverse phenotypes were simultaneously separated from ECs and U87 cell line. PNCs, GCs(H) and U87(H) exhibited longer cellular protrusion than ECs, GCs(L) and U87(L), respectively. Cell strains with longer protrusion exhibited higher invasive ability and lower sensitivity to temozolomide (TMZ) and radiation. Subsequently, TPD52L2 was verified as the functional protein to regulate the cellular heterogeneity by the proteomics analysis. Downregulation of TPD52L2 enhanced cell invasion whereas inhibited cell proliferation rate and sensitivity to chemotherapy in vivo and in vitro, this condition was reversed when TPD52L2 was overexpressed. The invasiveness was facilitated by up-regulating CTNNB1/β-catenin and SNAI1/Snail mediated EMT process. In addition, the clinical data of 88 GBM cases in our neurosurgery center was analyzed to reveal the influence of TPD52L2 in the prognosis of GBM. Low expression of TPD52L2 exacerbated prognosis of GBM patients received standard radiotherapy plus concomitant and adjuvant TMZ (Stupp strategy). Taken together, TPD52L2 is an important biomarker influencing GBM prognosis. 

Retracted: No

PubPeer comments:
 Duplication between figures 2B and 3G. Appears to be the same image with stretching and contrast adjustment. ![file] ![file] ,