Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial‑mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells.
Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial‑mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells.
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长链非编码RNA KCNQ1OT1通过调节晶状体上皮细胞中的SMAD4促进增殖和上皮间质转化
DOI：
10.3892/mmr.2018.8987
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发表时间：
2018-07
影响因子：
3.4
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Chen B;Ma J;Li C;Wang Y
长链非编码RNA（lncRNA）与包括白内障在内的各种疾病相关。lncRNA钾电压门控通道亚家族Q成员1反链/反义转录本1（KCNQ 1 OT 1）在白内障疾病中对透镜上皮细胞（LEC）增殖和上皮间质转化（EMT）的作用尚不清楚。在本研究中，KCNQ 1 OT 1和母亲对decapentaplegic同源物（SMAD）4的表达水平上调人类白内障透镜后囊样本和转化生长因子（TGF）-β2处理的SRA 01/04细胞，如通过逆转录定量聚合酶链反应，免疫组织化学染色和蛋白质印迹分析。进一步的功能丧失试验显示，抑制KCNQ 1 OT 1抑制TGF-β2处理的SRA 01/04细胞的增殖和EMT。另外，本研究还发现KCNQ 1 OT 1的增加和减少可调控SMAD 4的表达，提示SMAD 4可能是KCNQ 1 OT 1的下游基因。最后，构建SMAD 4 RNA干扰实验，证实KCNQ 1 OT 1的功能是通过SMAD 4信号通路作用于LEC增殖和EMT。本研究为白内障的分子治疗提供了新的靶点。
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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影响因子：
2
作者：
Liu L;Xiao W
通讯作者：
Xiao W
影响因子：
4.6
作者：
Sunamura N;Ohira T;Kataoka M;Inaoka D;Tanabe H;Nakayama Y;Oshimura M;Kugoh H
通讯作者：
Kugoh H
影响因子：
5.3
作者：
Gong W;Zheng J;Liu X;Liu Y;Guo J;Gao Y;Tao W;Chen J;Li Z;Ma J;Xue Y
通讯作者：
Xue Y
DOI：
10.1042/bcj20160128
发表时间：
2016-05-15
期刊：
The Biochemical journal
影响因子：
--
作者：
Nahomi RB;Pantcheva MB;Nagaraj RH
通讯作者：
Nagaraj RH
Dickkopf-1抑制Wnt3a诱导的人晶状体上皮细胞迁移和上皮间质转化
影响因子：
3.4
作者：
Liu, Tingting;Zhang, Limin;Bao, Xiuli
通讯作者：
Bao, Xiuli