@Article{biocell.2022.016167,
AUTHOR = {XUE JIANG, HONG ZHANG},
TITLE = {Knockdown of lncRNA XIST prevents the epithelial-mesenchymal transition of TGF-β2-induced human lens epithelial cells via miR-124/Slug axis},
JOURNAL = {BIOCELL},
VOLUME = {46},
YEAR = {2022},
NUMBER = {3},
PAGES = {785--794},
URL = {http://www.techscience.com/biocell/v46n3/45619},
ISSN = {1667-5746},
ABSTRACT = {Posterior capsular opacification (PCO) is linked to the pathological process of lens epithelial cells, which includes proliferation, migration, and epithelial-mesenchymal transition (EMT). Our goal was to investigate whether long noncoding RNA (lncRNA) XIST contributes to EMT via targeting miR-124/Slug axis in TGF-β2-induced SRA01/04 cells. EMT was induced by stimulating SRA01/04 cells with 10 ng/mL TGF-β2 for 24 h, and PCO microenvironment was simulated. The expressions levels of lncRNA XIST, miR-124, and Slug were measured by real-time polymerase chain reaction (RT-PCR) and western blot. The role and mechanism of lncRNA XIST in promoting EMT of TGF-β2-treated SRA01/04 cells were investigated by using cell transfection, cell counting kit-8 (CCK-8), immunofluorescence staining, transwell assay, wound-healing assay, RT-PCR, western blot and dual-luciferase reporter assay. The expression of Slug and lncRNA XIST was markedly increased, while miR-124 was downregulated in TGF-β2-treated SRA01/04 cells compared with the control group. Knockdown of lncRNA XIST reduced EMT, migration, and cell viability in TGF-β2-induced SRA01/04 cells; moreover, it adversely modulated miR-124 and adjusted the expression of Slug in SRA01/04 cells, while these effects were diminished by co-transfection with AMO-miR-124. Our data demonstrated that lncRNA XIST functioned as a competitive endogenous RNA (ceRNA) of miR-124 to modulate the expression level of Slug, thereby modulating EMT, migration, and cell viability in SRA01/04 cells. In conclusion, lncRNA XIST has a crucial role in promoting TGF-β2-induced EMT via modulating the miR-124/Slug axis in SRA01/04 cells, and it may provide a novel therapeutic option for PCO treatment.},
DOI = {10.32604/biocell.2022.016167}
}