MicroRNA-146a Regulates the Epithelium-Mesenchymal Transition of Lens Epithelial Cells Through the STAT1/MYC Pathway.

PURPOSE: This study aimed to elucidate the effects and mechanisms of microRNA-146a on the proliferation, apoptosis, migration, and epithelial-mesenchymal transition (EMT) of human lens epithelial cells (HLECs).

METHODS

Anterior capsular tissue obtained during surgery from the age-related cataract (ARC) group and the control group was collected; the tissue was ground and subjected to RT-qPCR experiments to analyze the expression of microRNA-146a; in in vitro experiments, TNF-α (20 ng/ml) induced human lens epithelial cells (HLECs) to establish an inflammatory injury cell model; Transfection of TNF-α-treated HLECs with microRNA-146a mimics and STAT1 overexpression plasmid; RT-qPCR, Western The blotting method was used to detect the mRNA and protein expression levels of EMT markers (E-cadherin, Vimentin, a-SMA) after cell treatment; the transwell assay and cell scratch experiment were used to detect changes in the migration ability of cells after treatment; the CCK8 assay was used to detect cell proliferation after treatment Changes in ability; flow cytometry was used to detect changes in cell apoptosis before and after cell treatment. RT-qPCR and Western blotting were used to detect the STAT1/MYC pathway mRNA and protein expression levels after cell treatment.

RESULTS

The expression of microRNA-146a in the capsules of patients with age-related cataracts was lower than that in the control group, and the mRNA expression of TNF-α was significantly higher than that in the control group. Induction by TNF-α (20 ng/ml) can cause inflammatory damage to normal HLECs and significantly change the expression of microRNA-146a and EMT-related genes in HLECs. Overexpression of microRNA-146a reverses TNF-α-induced EMT in HLECs. microRNA-146a affects the STAT1/MYC pathway by targeting and regulating STAT1.

CONCLUSION

MicroRNA-146a directly targets STAT1 and inhibits TNF-α-induced proliferation, migration, and EMT of lens epithelial cells through the STAT1/MYC pathway, exerting a protective effect.