lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis
- Chao Wang
- Ruiling Zhao
- Suhong Zhang
Affiliations: Department of Ophthalmology, Shandong Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277100, P.R. China, Department of Ophthalmology, Shandong Tengzhou Central People's Hospital, Zaozhuang, Shandong, 277599, P.R. China
- Published online on: November 8, 2021 https://doi.org/10.3892/mmr.2021.12523
Copyright: © Wang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License [CC BY_NC 4.0].
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
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.