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  2. 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

  • Chem Biodivers. 2019 Aug;16(8):e1900325. doi: 10.1002/cbdv.201900325.
Yingxiang Liu 1 2 Ziting Ren 1 2 Xiang Li 1 Jing Zhong 1 3 Yun Bi 1 Rui Li 1 2 Qun Zhao 1 Xianjun Yu 1 4
Affiliations

Affiliations

  • 1 Laboratory of Inflammation and Molecular Pharmacology, School of Basic Medical Sciences & Biomedical Research Institute, Hubei University of Medicine, Shiyan, 442000, P. R. China.
  • 2 First Clinical College, Hubei University of Medicine, Shiyan, 442000, P. R. China.
  • 3 Hubei Key Laboratory of Natural Products Research and Development, China Three Gorges University, Yichang, 443002, P. R. China.
  • 4 Institute of Medicine and Nursing, Hubei University of Medicine, Shiyan, 442000, P. R. China.
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.

Keywords

K562; ROS/JNK; apoptosis; autophagy; biological activity; pristimerin.

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