Open AccessGermacrone induces lung cancer cell apoptosis and cell cycle arrest via the Akt/MDM2/p53 signaling pathway
Author(s) -
Yang Zhao,
Jie Cai,
Kai-Hu Shi,
Hang Li,
Jin Du,
Dinghui Hu,
Zuntao Liu,
Wei Wang
Publication year - 2021
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2021.12091
Subject(s) - cell cycle , protein kinase b , apoptosis , cell cycle checkpoint , cancer research , oncogene , cell growth , signal transduction , biology , cell , tunel assay , viability assay , pi3k/akt/mtor pathway , mdm2 , microbiology and biotechnology , biochemistry
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 µ M GM significantly inhibited lung cancer cell proliferation, but significantly induced cell apoptosis and G 1 /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.