MicroRNA 483-3p suppresses the expression of DPC4/Smad4 in pancreatic cancer

被引：94

作者：

Hao, Jun ^{[1
]}

Zhang, Shuyu ^{[2
]}

Zhou, Yingqi ^{[1
]}

Hu, Xiangui ^{[1
]}

Shao, Chenghao ^{[1
]}

机构：

[1] Second Mil Med Univ, Changhai Hosp, Dept Pancreat Surg, Shanghai 200433, Peoples R China

[2] Soochow Univ, Coll Med, Sch Radiat Med & Publ Hlth, Suzhou 215123, Peoples R China

来源：

FEBS LETTERS | 2011年 / 585卷 / 01期

关键词：

Pancreatic cancer; miR-483-3p; DPC4/Smad4; GROWTH-FACTOR-BETA; TGF-BETA; INTRAEPITHELIAL NEOPLASIA; DPC4; INACTIVATION; SMAD PROTEINS; TRANSCRIPTION; PATHWAYS; PROMOTER; CELLS; PROGRESSION;

D O I：

10.1016/j.febslet.2010.11.039

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Both deregulation of tumor-suppressor genes and misexpression of microRNAs (miRNAs) have been implicated in the development of pancreatic cancer, but their relationship during this process remains less clear. Here, we report that the expression of miR-483-3p is strongly enhanced in pancreatic cancer tissues compared to side normal tissues using a miRNA-array differential analysis. Furthermore, DPC4/Smad4 is identified as a target of miR-483-3p and their expression levels are inversely correlated in human clinical specimens. Ectopic expression of miR-483-3p significantly represses DPC4/Smad4 protein levels in pancreatic cancer cell lines, and simultaneously promotes cell proliferation and colony formation in vitro. Our findings identify miR-483-3p as a potent regulator of DPC4/Smad4, which may provide a novel therapeutic strategy for the treatment of DPC4/Smad4-driven pancreatic cancer. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：207 / 213

页数：7