Gambogic acid improves non-small cell lung cancer progression by inhibition of mTOR signaling pathway

2Citations
Citations of this article
9Readers
Mendeley users who have this article in their library.

Abstract

Gambogic acid (GA) has been shown to inhibit cancer cell proliferation, induce apoptosis, and enhance reactive oxygen species accumulation. However, whether GA could improve multidrug resistance through modulating autophagy has never been explored. We demonstrated that the combination of GA and cisplatin (CDDP) resulted in a stronger growth inhibition effect on A549 and NCI-H460 cells using the MTT assay. Furthermore, treatment with GA significantly increased autophagy in these cells. More importantly, GA-induced cell death could be largely abolished by 3-methyladenine (3-MA) or chloroquine (CQ) treatment, suggesting that GA-induced cell death was dependent on autophagy. Western blot analysis showed that GA treatment suppressed the activation of Akt, mTOR, and S6. In addition, using a GA and rapamycin combination induced more cell death compared to either GA or rapamycin alone. In summary, GA may have utility as an adjunct therapy for non-small cell lung cancer (NSCLC) patients through autophagy-dependent cell death, even when cancer cells have developed resistance to apoptosis.

Cite

CITATION STYLE

APA

Zhao, T., Wang, H. J., Zhao, W. W., Sun, Y. L., & Hu, L. K. (2017). Gambogic acid improves non-small cell lung cancer progression by inhibition of mTOR signaling pathway. Kaohsiung Journal of Medical Sciences, 33(11), 543–549. https://doi.org/10.1016/j.kjms.2017.06.013

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free