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Pristimerin Induces Apoptosis and Autophagy via Activation of ROS/ASK1/JNK Pathway in Human Breast Cancer in Vitro and in Vivo

Pristimerin Induces Apoptosis and Autophagy via Activation of ROS/ASK1/JNK Pathway in Human Breast Cancer in Vitro and in Vivo

Qun Zhao, Yingxiang Liu, Jing Zhong, Yun Bi, Yongqiang Liu, Ziting Ren, Xiang Li, Junjun Jia, Mengting Yu, Xianjun Yu

Cell Death Discov. 2019 Aug 5;5:125.

PMID: 31396402

Abstract:

Breast cancer is the most common malignant tumor in women, and progress toward long-term survival has stagnated. Pristimerin, a natural quinonemethide triterpenoid, exhibits potential anti-tumor effects on various cancers. However, the underlying mechanism remains poorly understood. In this study, we found that pristimerin reduced the viability of breast cancer cells in vitro and the growth of xenografts in vivo, and these reductions were accompanied by thioredoxin-1 (Trx-1) inhibition and ASK1 and JNK activation. The results showed that pristimerin inhibited cell cycle progression and triggered cell apoptosis and autophagy. Furthermore, we found that the generation of reactive oxygen species (ROS) was a critical mediator in pristimerin-induced cell death. Enhanced ROS generation by pristimerin activated the ASK1/JNK signaling pathway. Inhibition of ROS with N-acetyl cysteine (NAC) significantly decreased pristimerin-induced cell death by inhibiting the phosphorylation of ASK1 and JNK. Taken together, these results suggest a critical role for the ROS/ASK1/JNK pathway in the anticancer activity of pristimerin.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP1258840	Pristimerin		1258-84-0	Price

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