The Proliferation Regulation Role of 17β-Estradiol-Induced miR-16-5p in Mouse Thymic Epithelial Cells

Abstract

Abstract To investigate the proliferation regulation role of 17β-Estradiol(E2)-induced miR-16-5p in mouse thymic epithelial cells. The miRNA expression profiles in the 50 nmo/L E2 treated MTEC1 cells were determined by high-throughput sequencing. Then the significantly upregulated miRNA expression that responsive to E2 was screened and validated. Subsequently, the proliferation functions and mechanism of screened miRNA were analyzed in MTEC1 cells. MiR-16-5p was found that significantly upregulated and had “high” levels of of expression among the 36 upregulation miRNAs, which were significantly induced by 50 nmol/L E2. Transfection assays showed that overexpression of miR-16-5p reduced cell viability, suppressed cell proliferation, and induced cell cycle arrest at the G0/G1 phase in MTEC1 cells. Results from further analysis confirmed CCND1 and Igfbp3 as the target genes of miR-16-5p, and that the effects of Igfbp3 knockdown were similar to those of miR-16-5p overexpression in MTEC1 cells. Moreover, it is similar to the roles of E2 affect MTEC1 cells proliferation, a significant up-regulation trend of miR-16-5p expression levels in MTEC1 cells was observed from 25 nmol/L to 50 nmol/L E2 after treatment for 6 h, 12 h, 24 h, and 48 h, respectively. This data indicated that the expression of miR-16-5p is an E2-responsive miRNA in MTEC1 cells, and also provided evidence that miR-16-5p has a proliferation role in MTEC1 cells proliferation. Suggests that E2 may affect thymic thymus involution by regulating the expression of miRNA in TECs.