ArticleMolecular medicine reports2022
lncRNA XIST knockdown suppresses cell proliferation and promotes apoptosis in diabetic cataracts through the miR‑34a/SMAD2 axis.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Expression and mechanistic roles of long non-coding RNAs in diabetic cataract: a systematic review and meta-analysis.Biology direct · 2026Pooled it
- Mechanistic and therapeutic perspectives of non-coding RNA-modulated apoptotic signaling in diabetic retinopathy.Cell biology and toxicology · 2024Review
- Plasma miR-19b, miR-34a, and miR-146a expression in patients with type 2 diabetes mellitus and cataract: A pilot study.Biomolecules & biomedicine · 2024Article
- Article
- Abnormal expression of lncRNA CASC9 in pneumonia children with respiratory failure and its feasible value for the clinical diagnosis of patients.Cell cycle (Georgetown, Tex.) · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.