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2018 ; 18
(1
): 16-24
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Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial?mesenchymal
transition by regulation of SMAD4 expression in lens epithelial cells
#MMPMID29749509
Chen B
; Ma J
; Li C
; Wang Y
Mol Med Rep
2018[Jul]; 18
(1
): 16-24
PMID29749509
show ga
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)??2?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??2?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.