Growing data have indicated that the miR-17–92 cluster is implicated in inflammatory response and rheumatoid arthritis(RA). This study was aimed to investigate the effects of miR-92a on the proliferation and migration of rheumatoid arthritisfibroblast-like synoviocytes (RA-FLSs). Our results showed that miR-92a was significantly down-regulated in RA synovialtissue and RA-FLSs, whereas the protein level of AKT2 is increased. Restoration of miR-92a suppressed the proliferationand migration of RA-FLSs. Down-regulation of miR-92a promotes proliferation and migration of normal human FLSs.Dual luciferase reporter gene assay showed that miR-92a could specifically bind with the 30UTR of AKT2 and significantlyrepressed the luciferase activity. Down-regulation or up-regulation of miR-92a significantly increased or decreased theprotein and phosphorylation levels of AKT2. siRNA-mediated down-regulation of AKT2 significantly prevented cellproliferation and migration of RA-FLSs, which were similar to the effects induced by overexpression of miR-92a.Moreover, AKT2 overexpression rescued miR-92a-mediated suppressive effect on proliferation and migration of RA-FLS.Thus, miR-92a could inhibit the proliferation and migration of RA-FLSs through regulation of AKT2 expression.
Volume 45, 2020
Continuous Article Publishing mode
Click here for Editorial Note on CAP Mode