Long non-coding RNA HOTAIR regulates the development of non-small cell lung cancer through miR-217/DACH1 signaling pathway.

Abstract

Long non-coding RNA HOX transcript antisense RNA (HOTAIR) is reported to make chromatin state, cell growth and cancer metastasis. However, the role of HOTAIR in non-small cell lung cancer (NSCLC) remains unknown. The aim of this study was to explore the regulatory mechanism of HOTAIR in NSCLC in relation to miR-217/Dachshund homolog 1 (DACH1) signaling pathway. The expression levels of HOTAIR and miR-217 were measured by quantitative Polymerase Chain Reaction (qPCR) in NSCLC cell lines and human bronchial epithelial cell line HBE. The direct target of HOTAIR and miR-217 in NSCLC was confirmed by a Luciferase reporter assay. The expression of DACH1 protein was examined by Western blot (WB) assay. Cell migration and invasion were examined with transwell assays, and cell proliferation was measured by Cell Counting Kit-8 (CCK8) assay. HOTAIR was up-regulated and miR-217 was down-regulated in NSCLC cell lines. Silencing of HOTAIR significantly repressed cell proliferation and inhibited cell migration and invasion in H1299 and A549 cells by facilitating miR-217 expression. Moreover, bioinformatics analysis and Luciferase reporter assay confirmed that DACH1 was a target of miR-217. Furthermore, the overexpression of miR-217 markedly repressed cell proliferation and inhibited cell migration and invasion in H1299 and A549 cells. DACH1 reverses the effects of miR-217 overexpression in NSCLC cells. HOTAIR was up-regulated in NSCLC cell and regulates the proliferation, migration, invasion through the miR-217/DACH1 signaling pathway. It provides a novel potential treatment strategy for NSCLC.