文献类型：期刊文献

英文题名：MiR-139 inhibits invasion and metastasis of colorectal cancer by targeting the type I insulin-like growth factor receptor

作者：Shen, Ke[2,3];Liang, Qiannan[2,3];Xu, Ke[2,3];Cui, Daling[2,3];Jiang, Lin[2,3];Yin, Peihao[1];Lu, Yanhua[2,3];Li, Qi[1];Liu, Jianwen[2,3]

机构：[1]Putuo Hosp Shanghai Univ Tradit Chinese Med, Dept Oncol, Shanghai 201203, Peoples R China;[2]E China Univ Sci & Technol, Sch Pharm, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[3]E China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab New Drug Design, Shanghai 200237, Peoples R China

年份：2012

卷号：84

期号：3

起止页码：320

外文期刊名：BIOCHEMICAL PHARMACOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000305546200009)】；

基金：This work was supported by the Shanghai Committee of Science and Technology (grant 11DZ2260600) and the Fundamental Research Funds for the Central Universities.

语种：英文

外文关键词：miR-139; CRC; Metastasis; Invasion; IGF-IR

摘要：MicroRNAs (miRNAs), which are noncoding RNAs that regulate gene expression, are involved in tumor metastasis. In this study, we describe the down-regulation and function of miR-139 in colorectal cancer (CRC) metastasis. MiR-139 was found underexpressed in 34 CRC tissues compared to their corresponding nontumor tissues. Decreased miR-139 in CRC tissue was associated with disease progression and metastasis. Re-expression of miR-139 did not inhibit CRC cell growth but suppresses CRC cell metastasis and invasion in vitro and in vivo. MiR-139 might suppress CRC cells invasion and metastasis by targeting type I insulin-like growth factor receptor (IGF-IR). We also found miR-139 directed migration inactivation of human CRC cells involves down-regulation of matrix metalloproteinase 2 (MMP-2). The IGF-IR/MEK/ERK signaling was inhibited by miR-139 overexpression and then resulted in MMP-2 promoter suppression. Taken together, our results provide evidence that miR-139 might function as a metastasis suppressor in CRC. Targeting miR-139 may provide a strategy for blocking CRC metastasis. (C) 2012 Elsevier Inc. All rights reserved.