| Literature DB >> 25628794 |
Kai Huang1, Xiyuan Dong1, Cong Sui1, Dan Hu1, Ting Xiong1, Shujie Liao1, Hanwang Zhang1.
Abstract
MicroRNAs were recently found to participate in oncogenesis and growth of various tumors. We hypothesized that microRNA-223 (miR-223) plays a role in endometrial carcinoma growth. In this study, we transfected RL95-2 cells with lentivirus containing miR-223 precursor to establish a miR-223 over-expression model. Proliferation of the cells was greatly inhibited when miR-223 was over-expressed, and cell cycle progress was blocked in G0/G1 phase. To investigate the mechanisms involved, we scanned the putative target genes of miR-223 using bioinformatics, and confirmed that insulin-like growth factor-1 receptor (IGF-1R) was a functional target of miR-223 using quantitative PCR, Western blot and luciferase reporter assay. Meanwhile, over-expressed miR-223 was found to regulate the expression of IGF-1R by repressing protein translation. Silencing IGF-1R with small interfering RNA resulted in similar effect as miR-223 overexpression. Therefore, our data suggest that miR-223 regulates RL95-2 cells proliferation and cell cycle progress by targeting IGF-1R.Entities:
Keywords: MiR-223; cell proliferation; endometrial carcinoma cell; in vitro; insulin-like growth factor-1 receptor
Year: 2014 PMID: 25628794 PMCID: PMC4297351
Source DB: PubMed Journal: Am J Transl Res Impact factor: 4.060