XIST promote the proliferation and migration of non-small cell lung cancer cells via sponging miR-16 and regulating CDK8 expression.

Up-regulation of long non-coding RNA (lncRNA) XIST has been observed in the tissue samples of non-small cell lung cancer (NSCLC), however, the underlying mechanisms remain uncertain. The aim of this study is to investigate the roles of XIST in the pathogenesis of NSCLC and the underlying mechanism. We noted that XIST in NSCLC tumor tissue and cell lines was significantly up-regulated. XIST over-expression promoted the proliferation and migration, meantime, increased the proportion of cells in the S phase in NSCLC cell line A549 and H1299. Meantime, knockdown of XIST showed the opposite effects. In vivo study further revealed a oncogenic effect of XIST. In addition, we conducted bioinformatics analysis and luciferase activity assay to find out the potential target miR of XIST and the potential target gene of miR-16 which is CDK8. In conclusion, our findings proved that XIST can serve as a tumor promoter in the pathogenesis of NSCLC, suggesting that XIST has the potential to become a novel therapeutic target for the treatment of NSCLC. AJTR