MicroRNA miR-29c-3p modulates FOS expression to repress EMT and cell proliferation while induces apoptosis in TGF-β2-treated lens epithelial cells regulated by lncRNA KCNQ1OT1.

Abstract

Age-related cataract (ARC) is a main cause of blindness for elderly people. MicroRNA hsa_miR-29c-3p (miR-29c-3p) was implicated in many biological processes in complicated diseases. However, the biological mechanism of miR-29c-3p in ARC is still undefined. Quantitative real-time polymerase chain reaction (qRT-PCR) showed that miR-29c-3p was lowly expressed, while FBJ murine osteosarcoma viral oncogene homolog (FOS) and KCNQ1 overlapping transcript 1 (KCNQ1OT1) were highly expressed in cataract tissues and in TGF-β2-treated SRA01/04 cells. Western blot assay indicated that TGF-β2 could promote epithelial-mesenchymal transition (EMT). Moreover, our data suggested that miR-29c-3p overexpression suppressed EMT, cell proliferation and promoted apoptosis in TGF-β2-treated SRA01/04 cells. The dual-luciferase reporter assay verified that FOS was a target of miR-29c-3p and miR-29c-3p was directly targeted by KCNQ1OT1. Furthermore, KCNQ1OT1 could regulate FOS expression by sponging miR-29c-3p. Functional assays revealed that miR-29c-3p regulated FOS to repress EMT, cell proliferation and facilitate apoptosis in TGF-β2-treated SRA01/04 cells mediated by KCNQ1OT1. In conclusion, KCNQ1OT1/miR-29c-3p/FOS axis played a vital role in the progression of ARC.