Alisol B 23‑acetate inhibits the viability and induces apoptosis of non‑small cell lung cancer cells via PI3K/AKT/mTOR signal pathway.

Abstract

The aim of the present study was to investigate the effects of alisol B 23-acetate (AB23A) on inhibiting the viability and inducing apoptosis of human non-small cell lung cancer (NSCLC) cells and the anticancer mechanisms of AB23A in vitro. The viability of A549 cells following treatment with different doses of AB23A was examined using a Cell Counting Kit-8 assay. Subsequently, apoptosis and the cell cycle were detected using flow cytometric analysis. The effect of AB23A on migration and invasion of A549 cells was detected by wound healing and Transwell assays. Western blotting was performed to determine the relative expression of Bax/Bcl-2, phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) and mammalian target of rapamycin (mTOR). AB23A markedly inhibited the viability enhanced apoptosis of A549 cells and arrested the cell cycle in G1 phase. Additionally, AB23A upregulated the ratio of Bax/Bcl-2 in the A549 cells in a concentration-dependent manner. The results of wound healing and Transwell assays indicated that AB23A also suppresses the migration and invasion ability of A549 cells. Furthermore, AB23A reduced the protein levels of phosphorylated AKT, PI3K and mTOR. In conclusion, AB23A exerted anti-cancer activity via inhibiting cells viability, migration and invasion, and promoting apoptosis. Therefore, AB23A is a potential antitumor drug for the treatment of NSCLC.