Maslinic acid induces autophagy through PI3K/Akt/mTOR pathway in human nasopharyngeal carcinoma cells
10.7501/j.issn.0253-2670.2020.09.024
- VernacularTitle: 山楂酸通过PI3K/Akt/mTOR通路诱导鼻咽癌CNE2细胞自噬研究
- Author:
Fang-Liang ZHOU
1
Author Information
1. College of Medicine, Hunan University of Chinese Medicine
- Publication Type:Journal Article
- Keywords:
Autophagy;
Cell proliferation;
Maslinic acid;
Nasopharyngeal carcinoma;
PI3K/Akt/mTOR
- From:
Chinese Traditional and Herbal Drugs
2020;51(9):2481-2485
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of maslinic acid (MA) on the proliferation and autophagy in nasopharyngeal carcinoma CNE2 cells and to elucidate the regulatory role of PI3K/Akt/mTOR pathway in this process. Methods: The effect of MA on the proliferation of CNE2 cells was assessed by CCK-8. MDC staining of autophagic vacuoles was performed for autophagy analysis. Additionally, the levels of autophagy-and PI3K/Akt/mTOR-associated proteins were examined using western blot analysis. Results: MA significantly inhibited the proliferation of CNE2 cells in a dose-and time-dependent manner. MA displayed autophagy-inducing effect, as shown by the increased MDC-labeled vacuoles, up-regulated LC3-II/LC3-I ratio and Atg5, as well as the down-regulated p62 level after MA treatment. Moreover, we observed that MA inhibited the expression of PI3K-p110α and the phosphorylation of Akt and mTOR. Conclusion: MA inhibits the proliferation and induces the autophagy of CNE2 cells, the mechanism may be related to the PI3K/Akt/mTOR signaling pathway. These results imply that MA may be a potential anti-cancer agent for use in the treatment of nasopharyngeal carcinoma.
