Long - Chain Non - Coding RNAANRIL Inhibits The Expression Of KLF2 And P21 And Affects The Proliferation And Apoptosis Of NSCLC Cells

Recent evidence highlight long non-coding RNAs(lnc RNAs) as crucial regulators of cancer biology, which contribute to essential cancer cell functions such as cell proliferation, apoptosis and metastasis. In non small cell lung cancer(NSCLC), several lnc RNAs expression are misregulated and have been nominated as critical actors in NSCLC tumorigenesis. Lnc RNA ANRIL was firstly found to be required for the PRC2 recruitment to and silencing of p15INK4 B, which expression is induced by ATM-E2F1 signaling pathway. Our previous study showed that ANRIL was significantly up-regulated in gastric cancer, and it could promote cell proliferationand inhibit cell apoptosis by silencing of mi R-99 a and mi R-449 a transcription. However, its clinical significance and potential role in NSCLC is still not documented. In this study, we reported that ANRIL expression was increased in NSCLC tissues and Its expression level was significantly correlated with TNM stages and tumor size. Moreover, patients with high levels of ANRIL expression had a relatively poor prognosis. In addition, taking advantage of loss of function experiments in NSCLC cells, we found that knockdown of ANRIL expression could impair cell proliferation and induce cell apoptosis both in vitro and vivo. Furthermore, we uncover that ANRIL could not repress p15 expression in PC9 cells, but through silencing of KLF2 and P21 transcription. Thus, we conclusively demonstrate that lnc RNA ANRIL plays an key role in NSCLC development by associating its expression with survival in NSCLC patients, providing novel insights on the function of lnc RNA-driven tumorigenesis.