LAUSR

In this study, we mainly focus on probing expression profile and detailed functions of long non coding RNA TFAP2A antisense RNA 1 (TFAP2A AS1) in non small cell lung cancer (NSCLC). Moreover, the mechanisms played by TFAP2A AS1 were unraveled comprehensively. Herein, a notable overexpressed TFAP2A AS1 in NSCLC was observed by TCGA and our own cohort. An increased TFAP2A AS1 level displayed a negative correlation with the overall survival of patients with NSCLC. Loss of function approaches illustrated that the absence of TFAP2A AS1 weakened NSCLC cell proliferation, colony formation, migration and invasion in vitro. Also, interference of TFAP2A AS1 caused in vivo tumor growth suppression. Mechanistically, TFAP2A AS1 could negative regulate microRNA 584 3p (miR 584 3p) as a competitive endogenous RNA. Furthermore, cyclin dependent kinase 4 (CDK4), a direct target of miR 584 3p, was positively controlled by TFAP2A AS1 in a miR 5184 3p dependent manner. Rescue function experiments corroborated that the anticancer activities of TFAP2A AS1 deficient on the oncogenicity of NSCLC cells were reversed by downregulating miR 584 3p or overexpressing CDK4. To sum up, TFAP2A AS1 exhibits cancer promoting roles in NSCLC through the adjustment of miR 584 3p/CDK4 axis.