Down-regulation of lncRNA-ATB inhibits epithelial-mesenchymal transition of breast cancer cells by increasing miR-141-3p expression.

Long noncoding RNA activated by transforming growth factor-beta (lnc-ATE) is abnormally expressed in a number of tumor types. The aim of this study was to investigate the expression of lnc-ATE and miR-141-3p, and to determine whether lnc-ATE can regulate epithelial-mesenchymal transition (EMT) by mi R-141-3p in breast cancer. Here, we found that Inc-ATE was highly expressed, whereas there was low expression of miR-141-3p in breast cancer tissues and cells. Knockdown of lnc-ATE in two breast cancer cell lines (MDA-MB-231 and BT549) significantly increased miR-141-3p expression. Down-regulation of lnc-ATE 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-ATE 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-ATE significantly inhibits the EMT process of breast cancer cells by increasing the expression of miR-141-3p, indicating that Inc-ATE might serve as a novel therapeutic target for breast cancer.