Indexed on: 07 Jan '17Published on: 07 Jan '17Published in: Oncology research
Previous studies reported that elevated expression of long noncoding RNA GAS5 led to NSCLC cell growth arrest and a promotion of apoptosis both <em>in vitro</em> and <em>in vivo</em>. However, its underlying molecular mechanism in NSCLC is still unclear. In the present study, we noted that GAS5 was down-regulated in NSCLC tissues and cells and was negatively correlated with miR-23a expression. Luciferase reporter assay and qRT-PCR analysis demonstrated that GAS5 directly interacted with miR-23a and reversely regulate its expression. miR-23a overexpression markedly promoted NSCLC cell proliferation and invasion, while GAS5 overexpression dramatically inhibited NSCLC cell proliferation, invasion and promoted apoptosis. Function analysis indicated that miR-23a overexpression significantly abolished GAS5 overexpression-induced inhibition of proliferation and invasion, as well as promotion of apoptosis in NSCLC cells. Moreover, xenografts experiments further revealed up-regulation of GAS5 notably impaired the growth of transplanted tumor by suppressing miR-23a in nude mice. These results suggested that overexpression of lncRNA GAS5 inhibits tumorigenesis of NSCLC by inhibiting miR-23a <em>in vitro</em> and <em>in vivo</em>, providing a potential therapeutic strategy for patients with NSCLC.