Long non-coding RNA XIST promotes TGF-β-induced epithelial-mesenchymal transition by regulating miR-367/141-ZEB2 axis in non-small-cell lung cancer

Growing evidence shows that IncRNA XIST functions as an oncogene accelerating tumor progression. Transforming growth factor beta (TGF-beta)-induced epithelial-mesenchymal transition (EMT) plays a key role in tumor metastasis. However, it is still unclear whether IncRNA XIST is implicated in TGF-beta-induced EMT and influences cell invasion and metastasis in non-small-cell lung cancer (NSCLC). Here, we observed increased expression of IncRNA XIST and ZEB2 mRNA in metastatic NSCLC tissues. Knockdown of IncRNA XIST inhibited ZEB2 expression, and repressed TGF-beta-induced EMT and NSCLC cell migration and invasion. Being in consistent with the in vitro findings, the in vivo experiment of metastasis showed that knockdown of IncRNA XIST inhibited pulmonary metastasis of NSCLC cells in mice. In addition, knockdown of ZEB2 expression can inhibit TGF-beta-induced EMT and NSCLC cell migration and invasion. Mechanistically, IncRNA XIST and ZEB2 were targets of miR-367 and miR-141. Furthermore, both miR-367 and miR-141 expression can be upregulated by knockdown of IncRNA XIST. Taken together, our study reveals that IncRNA XIST can promote TGF-beta-induced EMT and cell invasion and metastasis by regulating miR-367/miR-141-ZEB2 axis in NSCLC. (C) 2018 Elsevier B.V. All rights reserved.