MicroRNA-495 induces breast cancer cell migration by targeting JAM-A.
10.1007/s13238-014-0088-2
- Author:
Minghui CAO
1
;
Weiwei NIE
;
Jing LI
;
Yujing ZHANG
;
Xin YAN
;
Xiaoxiang GUAN
;
Xi CHEN
;
Ke ZEN
;
Chen-Yu ZHANG
;
Xiaohong JIANG
;
Dongxia HOU
Author Information
1. State Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for microRNA Biology and Biotechnology, School of Life Sciences, Nanjing University, Nanjing, 210093, China.
- Publication Type:Journal Article
- MeSH:
3' Untranslated Regions;
genetics;
Adult;
Aged;
Blotting, Western;
Breast Neoplasms;
genetics;
metabolism;
pathology;
Cell Adhesion Molecules;
genetics;
metabolism;
Cell Line, Tumor;
Cell Movement;
genetics;
Female;
Gene Expression Regulation, Neoplastic;
Gene Knockdown Techniques;
Humans;
MCF-7 Cells;
MicroRNAs;
genetics;
Middle Aged;
RNA Interference;
Receptors, Cell Surface;
genetics;
metabolism;
Reverse Transcriptase Polymerase Chain Reaction
- From:
Protein & Cell
2014;5(11):862-872
- CountryChina
- Language:English
-
Abstract:
MicroRNAs (miRNAs) are small, non-coding RNAs that function as post-transcriptional regulators of gene expression. The deregulated expression of miRNAs is associated with a variety of diseases, including breast cancer. In the present study, we found that miR-495 was markedly up-regulated in clinical breast cancer samples by quantitative real time-PCR (qRT-PCR). Junctional adhesion molecule A (JAM-A) was predicted to be a potential target of miR-495 by bioinformatics analysis and was subsequently verified by luciferase assay and Western blotting. JAM-A was found to be negatively correlated with the migration of breast cancer cells through loss-of-function and gain-of-function assays, and the inhibition of JAM-A by miR-495 promoted the migration of MCF-7 and MDA-MB-231 cells. Furthermore, overexpression of JAM-A could restore miR-495-induced breast cancer cell migration. Taken together, our findings suggest that miR-495 could facilitate breast cancer progression through the repression of JAM-A, making this miRNA a potential therapeutic target.
