circ-C20orf11 promotes karyopherin alpha 2 expression through miR-495-3p and affects non-small cell lung cancer development.

Abstract

Non-small cell lung cancer (NSCLC) progression is aggressive carrying a high risk of death. In the disease, little is known about the mechanism of circRNA (circ)-C20orf11, and further in-depth studies are needed. First, circ-C20orf11 expression in NSCLC was assessed, and the effects of circ-C20orf11 on NSCLC cell proliferative, apoptotic, migratory, and invasive behaviors were detected after transfection. The targeting relationship between miRNA (miR)-495-3p and circ-C20orf11 or recombinant karyopherin alpha 2 (KPNA2) was validated. We found circ-C20orf11 expression was elevated in NSCLC, and depleting circ-C20orf11 or restoring miR-495-3p hindered proliferative, migratory, and invasive behaviors of NSCLC cells and stimulated apoptosis, while enhancing circ-C20orf11 or silencing miR-495-3p showed the opposite effect. Moreover, the circ-C20orf11 could promote KPNA2 expression by sponging miR-495-3p, and overexpressing KPNA2 impaired the effect of circ-C20orf11 silencing on NSCLC cells. We conclude that circ-C20orf11 accelerates NSCLC via the miR-495-3p/KPNA2 axis.