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Pristimerin Induces Autophagy-Mediated Cell Death in K562 Cells Through the ROS/JNK Signaling Pathway

Pristimerin Induces Autophagy-Mediated Cell Death in K562 Cells Through the ROS/JNK Signaling Pathway

Yingxiang Liu, Ziting Ren, Xiang Li, Jing Zhong, Yun Bi, Rui Li, Qun Zhao, Xianjun Yu

Chem Biodivers. 2019 Aug;16(8):e1900325.

PMID: 31290253

Abstract:

Chronic myeloid leukemia (CML) is a lethal malignancy, and the progress toward long-term survival has stagnated in recent decades. Pristimerin, a quinone methide triterpenoid isolated from the Celastraceae and Hippocrateaceae families, is well-known to exert potential anticancer activities. In this study, we investigated the effects and the mechanisms of action on CML. We found that pristimerin inhibited cell proliferation of K562 CML cells by causing G1 phase arrest. Furthermore, we demonstrated that pristimerin triggered autophagy and apoptosis. Intriguingly, pristimerin-induced cell death was restored by an autophagy inhibitor, suggesting that autophagy is cross-linked with pristimerin-induced apoptosis. Further studies revealed that pristimerin could produce excessive reactive oxygen species (ROS), which then induce JNK activation. These findings provide clear evidence that pristimerin might be clinical benefit to patients with CML.

Chemicals Related in the Paper:

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

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