Silencing of CPSF7 inhibits the proliferation, migration, and invasion of lung adenocarcinoma cells by blocking the AKT/mTOR signaling pathway.

Abstract

Cleavage and polyadenylation specific factor 7 (CPSF7) is an important participator in the cleavage and polyadenylation of pre-mRNAs. This study aims to uncover the function and underlying mechanism of CPSF7 in lung adenocarcinoma (LUAD). CPSF7 expression in LUAD cells was measured using real time-quantitative polymerase chain reaction and Western blotting. Our results showed that CPSF7 expression was upregulated in LUAD cell lines (A549, H1299, and HCC827). To explore the function of CPSF7 on LUAD, CPSF7 was silenced by the si-CPSF7 transfection and overexpressed by the oe-CPSF7 transfection in A549 cells. Cell proliferation was measured using cell counting kit-8 and colony formation assays. Cell migration and invasion were measured by wound healing and Transwell assays, respectively. Our data revealed that CPSF7 silencing inhibited the viability, colony formation, migration, and invasion of LUAD cells. On the contrary, CPSF7 overexpression enhanced the malignant characteristics of LUAD cells. Additionally, expression of AKT/mTOR pathway-related proteins was detected using Western blotting. CPSF7 silencing blocked the AKT/mTOR signaling pathway. The intervention of SC79 (an activator of the AKT/mTOR pathway) weakened the antitumor effects of CPSF7 silencing in LUAD cells. Silencing of CPSF7 inhibits the malignant characteristics of LUAD cells by blocking the AKT/mTOR signaling pathway.