mi R-1181 inhibits invasion and proliferation via STAT3 in pancreatic cancer

作     者：Jie Wang Xing-Jun Guo You-Ming Ding Jian-Xin Jiang 

作者机构：Department of Hepatic-Biliary-Pancreatic Surgery The Affiliated Hospital of Guizhou Medical University Department of Biliary-Pancreatic Surgery Affiliated Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Department of Hepatic-Biliary-Pancreatic Surgery Renmin Hospital of Wuhan University 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2017年第23卷第9期

页      面：1594-1601页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：Supported by The National Natural Science Foundation of China No.81160311 and No.81572429 to Jiang JX 

主　　题：胰腺的癌症 miR-1181 增长 侵略 STAT3 

摘      要：AIM To examine the role of micro RNA 1181 (miR-1181) in invasion and proliferation in pancreatic cancer.METHODS We analyzed the expression of mi R-1181 in several pancreatic cancer cell lines and generated stable MIA-Pa Ca-2 and PANC-1 cell lines with up-regulated mi R-1181 expression using an adenovirus delivery system. We then investigated mi R-1181 s effect on invasion and proliferation of pancreatic cancer cells by transwell assay, wound healing assay, cell counting kit-8 assay and colony-forming assay, and explored any underlying mechanisms by western bolt. Beyond that, we observed the change of the PANC-1 cell s cytoskeleton by immunofluorescence staining.RESULTS Our data showed that mi R-1181 was relatively downregulated in pancreatic cancer cell lines compared with normal pancreatic ductal epithelial cells. And miR-1181 inhibited the migration, invasion and proliferation activities of MIA-Pa Ca-2 and PANC-1 cells. Notably,after over-expressing of mi R-1181 in PANC-1 cells, F-actin depolymerized. Immunofluorescence staining shows decreased F-actin and β-tubulin expression in PANC-1 cells over-expressing mi R-1181 compared with the control cells. Furthermore, we found that over-expressing mi R-1181 inhibited the expression of signal transducer and activator of transcription 3(STAT3) while knocking-down mi R-1181 up-regulated the expression of STAT3. Knocking-down mi R-1181 promoted the invasion and proliferation of pancreatic cancer cells. And inhibition of STAT3 blocked the promotion effects of knocking-down mi R-1181 on proliferation and invasion in pancreatic cancer. CONCLUSION Together our findings suggest that mi R-1181 may be involved in pancreatic cancer cell invasion and proliferation by targeting STAT3 and indicate that mi R-1181 may be a potential therapeutic agent for pancreatic cancer.