Germacrone induces lung cancer cell apoptosis and cell cycle arrest via the Akt/MDM2/p53 signaling pathway.

Abstract

Germacrone (GM) displays a wide range of antitumor, antioxidant and anti-inflammatory effects; however, to the best of our knowledge, the effects of GM on lung cancer cell apoptosis and cell cycle arrest have not been previously reported. The aim of the present study was to investigate discussed the effects of GM on the apoptosis and cycle arrest of lung cancer cells. Cell viability, proliferation and apoptosis were assessed by performing Cell Counting Kit-8, colony formation and TUNEL assays, respectively. Western blotting was performed to detect the expression levels of apoptosis-, cell cycle- and Akt/MDM2 proto-oncogene (MDM2)/p53 signaling pathway-related proteins. Compared with the control group, 50, 100 and 200 µM GM significantly inhibited lung cancer cell proliferation, but significantly induced cell apoptosis and G1/S cell cycle arrest. GM also significantly altered the expression levels of Akt/MDM2/p53 signaling pathway-related proteins compared with the control group. Administration of Akt activator SC79 significantly reversed GM-mediated antiproliferative, proapoptotic and pro-cell cycle arrest effects in lung cancer cells. Therefore, the results of the present study demonstrated that GM induced lung cancer cell apoptosis and cell cycle arrest via the Akt/MDM2/p53 signaling pathway.