Long Noncoding RNA Regulates the Proliferation, Migration, and Apoptosis of Human Venous Endothelial Cells Via SMYD3
Overview
Biotechnology
General Medicine
Affiliations
Numerous studies have shown that long noncoding RNAs (lncRNAs) play essential roles in the development and progression of human cardiovascular diseases. However, whether lncRNA ezrin antisense RNA 1 () is associated with the progression of coronary heart disease (CHD) remains unclear. Accordingly, the aim of the present study was to evaluate the role of lncRNA in patients with CHD and in human venous endothelial cells (HUVECs). The findings revealed that lncRNA was highly expressed in the peripheral blood of patients with CHD. experiments showed that the overexpression of could enhance proliferation, migration, and apoptosis by upregulating the expression of EZR in HUVECs; downregulation of lncRNA resulted in the opposite effect. lncRNA was also found to regulate SET and MYND domain-containing protein 3 (SMYD3), a histone H3 lysine 4-specific methyltransferase, which subsequently mediated EZR transcription. Collectively, these results demonstrate that lncRNA plays an important role in HUVECs function via SMYD3 signaling.
The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review.
Xie X, Huang M, Ma S, Xin Q, Wang Y, Hu L Noncoding RNA Res. 2025; 11:158-187.
PMID: 39896344 PMC: 11783329. DOI: 10.1016/j.ncrna.2024.12.009.
Role of LncRNAs in the Pathogenesis of Coronary Artery Disease.
Wu X, Li J, Sun G, Yang J, Peng Y, Bai X Rev Cardiovasc Med. 2024; 24(4):96.
PMID: 39076276 PMC: 11273030. DOI: 10.31083/j.rcm2404096.
Xu W, Shi L, Xu J, Qian H, Zhou H, Wang L Front Cell Dev Biol. 2023; 11:1125881.
PMID: 36968198 PMC: 10030596. DOI: 10.3389/fcell.2023.1125881.
Noncoding RNAs: emerging players in skin cancers pathogenesis.
Li L, Khan S, Li S, Wang S, Wang F Am J Cancer Res. 2021; 11(11):5591-5608.
PMID: 34873482 PMC: 8640824.
Lu D, Sun L, Li Z, Mu Z Mol Med Rep. 2020; 23(1).
PMID: 33236153 PMC: 7716411. DOI: 10.3892/mmr.2020.11714.