Abstract
Long noncoding RNAs (lncRNAs) are associated with various diseases including cataracts. The role of lncRNA potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) on lens epithelial cell (LEC) proliferation and epithelial-mesenchymal transition (EMT) in cataracts disease remains unclear. In the present study, KCNQ1OT1 and mothers against decapentaplegic homolog (SMAD)4 expression levels were upregulated in human cataract lens posterior capsular samples and in transforming growth factor (TGF)-β2-treated SRA01/04 cells, as demonstrated by reverse transcription-quantitative polymerase chain reaction, immunohistochemical staining and western blot analyses. A further loss of function test revealed that suppression of KCNQ1OT1 inhibited the proliferation and EMT of TGF-β2-treated SRA01/04 cells. Additionally, the present study reported that increase and decrease of KCNQ1OT1 regulated SMAD4 expression, which indicated that SMAD4 may be a downstream gene of KCNQ1OT1. Finally, a constructed SMAD4 RNA interference experiment confirmed that the function of KCNQ1OT1 was to act on LEC proliferation and EMT, and this was achieved via the SMAD4 signaling pathway. The findings of the present study may provide a novel target for molecular therapy of cataracts disease.
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