基因敲除
上皮-间质转换
癌症研究
波形蛋白
乳腺癌
生物
小RNA
癌症
化学
细胞培养
转移
基因
免疫学
免疫组织化学
遗传学
作者
Yang Zhang,Jianyi Li,Jia Song,Yitong Wang,Yuan Kang,Wenhai Zhang
标识
DOI:10.1139/bcb-2018-0168
摘要
Long noncoding RNA activated by transforming growth factor-beta (lnc-ATB) is abnormally expressed in a number of tumor types. The aim of this study was to investigate the expression of lnc-ATB and miR-141-3p, and to determine whether lnc-ATB can regulate epithelial–mesenchymal transition (EMT) by miR-141-3p in breast cancer. Here, we found that lnc-ATB was highly expressed, whereas there was low expression of miR-141-3p in breast cancer tissues and cells. Knockdown of lnc-ATB in two breast cancer cell lines (MDA-MB-231 and BT549) significantly increased miR-141-3p expression. Down-regulation of lnc-ATB resulted in a morphological change of breast cancer cells from spindle-like to a round shape, and in a remarkable inhibition of cell migration and invasion, which were reversed by miR-141-3p inhibitor. Furthermore, we demonstrated that lnc-ATB knockdown decreased ZEB1, ZEB2, N-cadherin, and vimentin expression, and promoted E-cadherin expression, while miR-141-3p inhibitor could reverse those effects. Moreover, we proved that miR-141-3p directly bound to the 3′ untranslated region (UTR) of ZEB1 and ZEB2 and negatively regulated ZEB1 and ZEB2 expression. Taken together, our results show that knockdown of lnc-ATB significantly inhibits the EMT process of breast cancer cells by increasing the expression of miR-141-3p, indicating that lnc-ATB might serve as a novel therapeutic target for breast cancer.
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