Circ_0017639 facilitates proliferative, migratory, and invasive potential of non-small cell lung cancer (NSCLC) cells via PI3K/AKT signaling pathway

Non-small cell lung cancer (NSCLC) has increased morbidity and mortality rate worldwide. The current NSCLS therapies are associated with poor outcomes and need further improvement. CircRNAs were shown to regulate NSCLC progression. However, little is known re garding the functions and mechanisms of circ_0017639 in NSCLC, which requires further extensive studies. The circ_0017639 expression in NSCLC tissues and cell lines was evaluated via qRT-RCR. Moreover, using ectopic plasmid incorporation and shRNA assays, we analyzed the circ_0017639-mediated cellular proliferative, migratory and invasive processes in NSCLC cell lines, using CCK-8, EdU, and transwell assays. Furthermore, the core proteins (p-PI3K, PI3K, p-AKT, and AKT) levels of the PI3K/AKT signaling cascade were investigated via immunoblotting. Finally, we tested the functional role of circ_0017639 by examining its regulation of xenograft tumor growths in nude mice in vivo. Circ_0017639 expression was remarkably high in the NSCLC tissues and cell lines. The transfection experiments showed that circ_0017639 overexpression was able to promote proliferative, migratory, and invasive properties of NSCLC cells, while sh-circ_0017639 showed opposing effects. We further showed that circ_0017639 knockdown suppressed the cellular development via PI3K/AKT cascade inactivation. Additionally, in-vivo experiment in nude mice demonstrated that sh-circ_0017639 could reduce the tumor growth of NSCLC. Circ_0017639 may promote the development of NSCLC by accelerating NSCLC metastasis through stimulating the PI3K/AKT cascade.