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

  • Authors:
    • Chao Wang
    • Ruiling Zhao
    • Suhong Zhang
  • View Affiliations / Copyright

    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
    Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 4.0].
  • Article Number: 7
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    Published online on: November 8, 2021
       https://doi.org/10.3892/mmr.2021.12523
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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.
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Copy and paste a formatted citation
Spandidos Publications style
Wang C, Zhao R and Zhang S: lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis. Mol Med Rep 25: 7, 2022.
APA
Wang, C., Zhao, R., & Zhang, S. (2022). lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis. Molecular Medicine Reports, 25, 7. https://doi.org/10.3892/mmr.2021.12523
MLA
Wang, C., Zhao, R., Zhang, S."lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis". Molecular Medicine Reports 25.1 (2022): 7.
Chicago
Wang, C., Zhao, R., Zhang, S."lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis". Molecular Medicine Reports 25, no. 1 (2022): 7. https://doi.org/10.3892/mmr.2021.12523
Copy and paste a formatted citation
x
Spandidos Publications style
Wang C, Zhao R and Zhang S: lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis. Mol Med Rep 25: 7, 2022.
APA
Wang, C., Zhao, R., & Zhang, S. (2022). lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis. Molecular Medicine Reports, 25, 7. https://doi.org/10.3892/mmr.2021.12523
MLA
Wang, C., Zhao, R., Zhang, S."lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis". Molecular Medicine Reports 25.1 (2022): 7.
Chicago
Wang, C., Zhao, R., Zhang, S."lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis". Molecular Medicine Reports 25, no. 1 (2022): 7. https://doi.org/10.3892/mmr.2021.12523
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