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Cucurbitacin I Induces Pro-Death Autophagy in A549 Cells via the ERK-mTOR-STAT3 Signaling Pathway

Cucurbitacin I Induces Pro-Death Autophagy in A549 Cells via the ERK-mTOR-STAT3 Signaling Pathway

Yinyun Ni, Sisi Wu, Xiangxiu Wang, Guonian Zhu, Xuemei Chen, Yu Ding, Wei Jiang

J Cell Biochem. 2018 Jul;119(7):6104-6112.

PMID: 29575175

Abstract:

Natural products are a great source of cancer chemotherapeutic agents. In the present study, the anticancer effects of cucurbitacin I on A549 cells were investigated. Cucurbitacin I decreased cell viability, inhibited colony formation, and induced apoptosis in A549 cells. Cucurbitacin I caused accumulation of autophagosome and dose-dependent expression of LC3II protein. Autophagy inhibitors 3-methyladenine (3-MA) inhibited autophagy induced by cucurbitacin I and relieved cucurbitacin I-triggered cell death and apoptosis in A549 Cells. Cucurbitacin I treatment inhibits the ERK activation and the downstream phosphorylation level of mTOR and STAT3, but not the PI3K/Akt pathway. Furthermore, treatment with the mTOR activator MHY-1485, which also suppressed cucurbitacin I-induced LC3II expression, and also reversed cucurbitacin I-induced cell death and apoptosis. Taken together, these results suggest that cucurbitacin I induced pro-death autophagy through ERK/mTOR/STAT3 signaling cascade in A549 cells.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP2222073-A	Cucurbitacin I		2222-07-3	Price

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