LncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis.

Abstract

According to emerging evidence, long non-coding RNAs (lncRNAs) play critical roles in diabetes. The aim of the present study was to investigate the role and mechanism of X-inactive specific transcript (XIST) in cell proliferation, migration and apoptosis in diabetic cataracts (DC). SRA01/04 lens epithelial cells were treated with high glucose (HG). The levels of XIST, microRNA (miR)-34a and SMAD family member 2 (SMAD2) were examined via reverse transcription-quantitative PCR. MTT, Transwell, wound healing and TUNEL assays were performed to examine cell proliferation, invasion, migration and apoptosis, respectively. The interaction between miR-34a and XIST or SMAD2 was verified by luciferase reporter assay. It was found that the expression of XIST was increased and that of miR-34a was decreased in DC tissues and HG-treated SRA01/04 cells. XIST knockdown or miR-34a overexpression attenuated cell proliferation and migration, and induced apoptosis in HG-treated SRA01/04 cells. XIST targeted miR-34a and regulated DC progression through miR-34a. SMAD2 was identified as a target gene of miR-34a and was positively modulated by XIST. XIST knockdown inhibited cell proliferation and migration, and accelerated apoptosis in HG-stimulated SRA01/04 cells, and these effects were abrogated by SMAD2 overexpression. In conclusion, XIST promoted cell proliferation, migration and invasion, and inhibited apoptosis, through the miR-34a/SMAD2 axis in DC.