文献类型：期刊文献

英文题名：Post-transcriptional regulation of the tumor suppressor miR-139-5p and a network of miR-139-5p-mediated mRNA interactions in colorectal cancer

作者：Shen, Ke[1,2];Mao, Rurong[1,2];Ma, Li[1,2];Li, Yueqi[1,2];Qiu, Yanyan[3];Cui, Daling[1,2];Le, Vanminh[1,2];Yin, Peihao[3];Ni, Lei[4];Liu, Jianwen[1,2]

机构：[1]E China Univ Sci & Technol, Dept Mol & Cellular Pharmacol, Biomed Nanotechnol Ctr, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]E China Univ Sci & Technol, Shanghai Key Lab New Drug Design, Sch Pharm, Shanghai 200237, Peoples R China;[3]Shanghai Univ Tradit Chinese Med, Putuo Hosp, Dept Gen Surg, Shanghai, Peoples R China;[4]Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Respirat, Shanghai 200030, Peoples R China

年份：2014

卷号：281

期号：16

起止页码：3609

外文期刊名：FEBS JOURNAL

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000340355400005)】；

基金：This work was supported by Shanghai Committee of Science and Technology (No. 13140902300), Nano Science and Technology Special Funding of the Shanghai Committee of Science and Technology (No. 11 nm0503700), 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：3'-UTR; colorectal cancer (CRC); competing endogenous RNA (ceRNA); miR-139-5p; post-transcriptional regulation

摘要：MicroRNAs play key roles in many biological processes, and are frequently dysregulated in tumor cells. However, there are few studies on how microRNAs are dysregulated. miR-139-5p, an important tumor suppressor, is often underexpressed in gastrointestinal cancer cells. Here, we describe post-transcriptional regulation of this intronic microRNA in human colorectal cancer. miR-139-5p is expressed independently of its overexpressed host gene PDE2A in colorectal cancer tissues and cell lines. The miR-139-5p target genes IGF1R, ROCK2 and RAP1B exert regulatory effects on the miR-139-5p expression level, relying on their ability to compete for miR-139-5p binding. These overexpressed target genes also regulate each others' protein levels through 3'-UTRs, thus regulating tumor cell growth and motility properties. Our study provides a mechanistic, experimentally validated rationale for intronic microRNA dysregulation in colorectal cancer, revealing novel oncogenic roles of IGF1R, ROCK2 and RAP1B 3'-UTRs.