贵州医科大学学报

2016, v.41;No.195(12) 1387-1392

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miRNA-1181通过抑制STAT3影响人胰腺癌细胞的侵袭转移能力
Capacity of miRNA to Influence the Migration and Invasion of Pancreatic Cancer through Inhibiting STAT3

王杰;喻超;周显飞;蔡坤;何志伟;江建新;
WANG Jie;YU Chao;ZHOU Xianfei;CAI Kun;HE Zhiwei;JIANG Jianxin;Department of Hepatic-Biliary-Pancreatic Surgery,the Affiliated Hospital of Guizhou Medical University;

摘要(Abstract):

目的:探讨miRNA-1181(miR-1181)对人胰腺癌细胞侵袭转移能力的影响以及机制。方法:选取胰腺癌细胞系PANC-1和MIA Pa Ca-2进行实验并构建miR-1181过表达慢病毒载体(miR-1181U),低表达慢病毒载体(miR-1181D)以及空载慢病毒载体(NC),采用实时荧光定量聚合酶链反应(qRT-PCR)检测感染效率;Transwell实验以及划痕实验检测miR-1181对胰腺癌细胞侵袭转移能力的影响,免疫荧光检测miR-1181对细胞骨架的影响,Western bolt检测STAT3的表达;构建si-STAT3并转染miR-1181低表达组(miR-1181D),重复transwell实验验证STAT3是其靶基因。结果:qRT-PCR显示3条不同序列的si-STAT3均能显著下调STAT3的表达;Transwell实验及划痕实验显示上调miR-1181后能显著抑制胰腺癌细胞的侵袭转移(P<0.05),下调miR-1181后能显著促进胰腺癌的侵袭转移(P<0.05);Western blot显示miR-1181U能抑制STAT3的表达,miR-1181D能促进STAT3的表达;免疫荧光显示在PANC-1细胞中过表达miR-1181后,F-肌动蛋白(F-actin)被剪切,呈现低表达,导致其运动结构和极性的缺失,从而迁移能力变弱;si-STAT3以后能减弱miR-1181D组对侵袭转移的促进作用。结论:miR-1181可能通过抑制STAT3来抑制人胰腺癌细胞的侵袭转移能力,有望成为胰腺癌治疗的潜在靶点。
Objective:To investigate the effect of microRNA-1181 on the migration and invasion of pancreatic cancer and its potential mechanism.Methods:Lentiviral vectors of miR-1181 including overexpression(miR-1181U),knockdown(miR-1181D) and a negative control(NC) were constructed,and were transfected into human pancreatic cancer cell lines PANC-1 and MIA-PaCa-2 respectively.The expressions of miR-1181 were detected by real-time PCR.Transwell assay and wound healing assay were employed to detect cell invasion ability.The influence of miR-1181 on cytoskeleton was detected with immunofluorescence technique,and the expression of STAT3 detected by Western bolt.siRNA for STAT3 was constructed and transfected into miR-1181 D,and then transwell assay was repeated to ensure that STAT3 was the miR-1181's target.Results:qRT-PCR results showed that 3 different si-STAT3 decreased expression of STAT3.Transwell assay and wound healing assay showed that miR-1181 U inhibited cell migration and invasion(P<0.05),and miR-1181 D promoted cell migration and invasion(P<0.05) significantly.Furthermore,miR-1181 U inhibited the expression of STAT3 while miR-1181 D up-regulated the expression of STAT3.Immunofluorescence test showed that when miR-1181 overexpressed in PANC-1 cells,F-actin was cut,and its expression was low.As the results,cells lost movement structure and polarity,and their migration capability was weakened.si-STAT3 can decrease the promotion effect of miR-1181 on migration and invasion in pancreatic cancer.Conclusion:miR-1181 may inhibit cell migration and invasion of pancreatic cancer by suppressing STAT3,which suggests it might be a potential new therapeutic agent for pancreatic cancer.

关键词(KeyWords): 胰腺肿瘤;miR-1181;肿瘤侵袭;肿瘤转移;STAT3
pancreatic neoplasms;miR-1181;tumor migration;tumor invasion;STAT3

Abstract:

Keywords:

基金项目(Foundation): 国家国际科技合作专项资助(2014DFA31420);; 国家自然科学基金(81160311,81572429,81660483)

作者(Author): 王杰;喻超;周显飞;蔡坤;何志伟;江建新;
WANG Jie;YU Chao;ZHOU Xianfei;CAI Kun;HE Zhiwei;JIANG Jianxin;Department of Hepatic-Biliary-Pancreatic Surgery,the Affiliated Hospital of Guizhou Medical University;

Email:

DOI: 10.19367/j.cnki.1000-2707.2016.12.005

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