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Lin D.,Soochow University of China | Liu C.,Soochow University of China | Xue M.,Soochow University of China | Liu R.,Soochow University of China | And 9 more authors.
PLoS ONE | Year: 2010

Background: Interleukin-15 (IL-15) plays important roles in the immune system and in the development of hematopoietic cells. Previous studies revealed that five SNPs in IL-15, rs10519612, rs10519613, rs35964658, rs17007695 and rs17015014, were significantly associated with childhood Acute Lymphoblastic Leukemia (ALL) treatment response. In adult ALL, the expression of IL-15 was also correlated with the immunophenotypes of ALL. Therefore, we hypothesize that SNPs of IL-15 might also be associated with adult ALL. Methods and Findings: We genotyped the above five SNPs of IL-15 gene by PCR-RFLP assays in adult ALL case-control studies. The current study included 121 adult ALL patients and 263 healthy controls. IL-15 genotypes and haplotypes were determined and the associations with the risk of ALL were analyzed by logistic regression. SNPs rs10519612 and rs17007695 were significantly associated with ALL (P = 0.013 and P = 0.001). We observed a 2-fold and 2.4-fold excess risk of developing ALL for the rs10519612 CC and rs17007695 TC genotype carriers compared with non-carriers, respectively. Haplotype analysis revealed that haplotypes ACAC, CAGT and CCAT were significantly associated with adult B-ALL, while haplotype CCAT conferred susceptibility to T-ALL. Conclusion: These findings suggest that IL-15 gene polymorphisms are significantly associated with ALL in adult Chinese population. ©2010 Lin et al.

Rong L.,The Peoples Hospital of Bozhou | Rong L.,Anhui University of Science and Technology | Hu D.,The Peoples Hospital of Bozhou | Wang W.,The Peoples Hospital of Bozhou | And 3 more authors.
Biomedical Research (India) | Year: 2016

To study the chemical constituents of Stephania kwangsiensis Lo. and to explore the effects of corydine on proliferation and apoptosis of lung adenocarcinoma NCI-H446 cells. Chemical structures were elucidated by MS, 1H-NMR and 13C-NMR. Effects of different concentrations of corydine on proliferation of lung adenocarcinoma NCI-H446 cells were determined by MTT assay. Effects of corydine on apoptosis rate of NCI-H446 cells were determined by flow cytometry. Three types of alkaloids were isolated from root tubers of Menispermaceae Stephania plant Stephania kwangsiensis Lo. Three different concentrations of corydine (20, 10, 5 Lg/ml) could all significantly increase the apoptosis rate of NCI-H446 cells after 48 h of treatment compared to the control group. Corydine can inhibit the proliferation of lung cancer NCI-H446 cells and induce their apoptosis. © 2016, Scientific Publishers of India. All rights reserved.

Chai P.,The Peoples Hospital of Bozhou | Tian J.,The Peoples Hospital of Bozhou | Zhao D.,The Hospital of Suzhou | Zhang H.,The Peoples Hospital of Bozhou | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2016

Gse1 coiled-coil protein (GSE1), also known as KIAA0182, is a proline rich protein. However, the function of GSE1 is largely unknown. In this study, we reported that GSE1 is overexpression in breast cancer and silencing of GSE1 significantly suppressed breast cancer cells proliferation, migration and invasion. Furthermore, GSE1 was identified as a direct target of miR-489-5p, which is significantly reduced in breast cancer tissues. In addition, forced expression of miR-489-5p suppressed breast cancer cells proliferation, migration and invasion. Moreover, depletion of GSE1 by siRNAs significantly abrogated the enhanced proliferation, migration and invasion of breast cancer cells consequent to miR-489-5p depletion. Taken together, these findings suggest that GSE1 may function as a novel oncogene in breast cancer and it can be regulated by miR-489-5p. © 2016.

Zhao T.-Y.,The Peoples Hospital of Bozhou | Tu J.,The Peoples Hospital of Bozhou | Wang Y.,The Peoples Hospital of Bozhou | Cheng D.-W.,The Peoples Hospital of Bozhou | And 7 more authors.
Asian Pacific Journal of Cancer Prevention | Year: 2016

Background: Through search the possible randomized control trials, we make a renewed meta-analysis in order to assess the impact of aspirin in preventing the recurrence of colorectal adenoma. Materials and Methods: The Medicine/PubMed, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), Chinese biomedical literature service system (SinoMed) databases were searched for the related randomized controlled trials until to the April 2016. Three different authors respectively evaluated the quality of studies and extracted data, and we used the STATA software to analyze, investigate heterogeneity between the data, using the fixed-effects model to calculate and merge data. Results: 7 papers were included the renewed metaanalysis, among these studies, two pairs were identified as representing the same study population, with the only difference being the duration of follow-up. Thus there were only five papers included our meta-analysis, and one Chinese paper were also included the work. Results were categorized by the length of follow-up, different kinds of people, varied dose of oral aspirin. The relative of adenoma in patients taking aspirin vs placebo were 0.73 (95% CI 0.55-0.98, P=0.039) with 1 year follow up; 0.84 (95% CI 0.72-0.98, P=0.484) with greater than 1 year follow up; for the advanced adenoma, the RR 0.68 (95% CI 0.49-0.94, P=0.582),for one year; RR=0.75 (95% CI 0.52-1.07, P=0.552) for greater one year. Furthermore the white population could divided into two subgroups according to the different length of follow-up time. When the length of follow-up time less than 3-year, The RR of two subgroups respective were RR=0.86 (95% CI 0.76-0.98, P=0.332), I2=0%, RR=0.68 (95% CI 0.47-0.98, P=0.552), I2=64.6%, But with the extension of follow-up time greater than 2-year, with the white, oral aspirin without considering dose had no efficacy on preventing the recurrence of any adenoma, the RR was 0.86 (95% CI 0.71-1.05, P=0.302), I2=16.4%. Conclusions: This meta-analysis indicated that oral aspirin is associated with a remarkable decrease in the recurrence of any adenoma and advanced adenomas in patients follow-up for 1 year without concerning the dose of aspirin, but with the extension of follow-up time for greater than 1 year, oral aspirin can be effective on preventing the recurrence of any adenoma, but for the advanced adenoma, the result indicated that oral aspirin had no efficacy, According to the inclusion of ethnic groups, we also divided relevant papers into two subgroups as the yellow and white group. Then the follow-up time was less than 3 years, oral aspirin without considering the dose, had an significant efficacy on preventing the recurrence of any adenoma. But with the follow-up greater than 2 years, oral aspirin had no effect in the white.

Li X.,The Peoples Hospital of Bozhou | Wang Y.,The Peoples Hospital of Bozhou | Wang H.,The Peoples Hospital of Bozhou | Huang C.,The Peoples Hospital of Bozhou | And 2 more authors.
Inflammation research : official journal of the European Histamine Research Society ... [et al.] | Year: 2015

OBJECTIVE: The objective of the review is to examine the crossroads of autophagy, inflammation, and apoptosis signaling pathways and their participation in liver fibrosis.INTRODUCTION: Endoplasmic reticulum (ER) stress was emerged as a common feature relevant to the pathogenesis of diseases associated with organ fibrosis. However, the functional consequences of these alterations on ER stress and the possible involvement in liver fibrosis were currently largely unexplored. Here, we will survey the recent literature in the field and discuss recent insights focusing on some cellular models expressing mutant proteins involved in liver fibrosis.METHODS: A computer-based online search with PubMed, Scopus and Web of Science databases was performed for articles published, concerning ER stress, adaptation, inflammation and apoptosis with relevance to liver fibrosis.RESULTS AND CONCLUSIONS: Progression of liver fibrosis requires sustained inflammation leading to hepatocytes apoptosis through ER stress, whereas associated with activation of hepatic stellate cells (HSCs) into a fibrogenic and proliferative cell type. Faced with persistent and massive ER stress, HSCs adaptation starts to fail and apoptosis occurs in reversal of liver fibrosis, possibly mediated through calcium perturbations, unfolded protein response, and the pro-apoptotic transcription factor CHOP. Although limited in scope, current studies underscored that ER stress is tightly linked to adaptation, inflammation and apoptosis, and recent evidences suggested that these processes are related to the pathogenesis of liver fibrosis and its recovery.

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