2. Academic Validation
  3. Typhaneoside prevents acute myeloid leukemia (AML) through suppressing proliferation and inducing ferroptosis associated with autophagy

Typhaneoside prevents acute myeloid leukemia (AML) through suppressing proliferation and inducing ferroptosis associated with autophagy

  • Biochem Biophys Res Commun. 2019 Sep 3;516(4):1265-1271. doi: 10.1016/j.bbrc.2019.06.070.
Hai-Yan Zhu 1,  Zong-Xuan Huang 2,  Guo-Qi Chen 3,  Fen Sheng 4,  Yin-Suo Zheng 5
Affiliations

Affiliations

  • 1 Department of the Frist Paediatrics, Ankang Central Hospital, Ankang, 725000, China.
  • 2 Department of Paediatrics, Affiliated Hospital of Jining Medical University, Jining, 272029, China.
  • 3 Department of Rehabilitation, Ankang Central Hospital, Ankang, 725000, China.
  • 4 Department of Intensive Care Unit, First People's Hospital of Jining, Shandong province, 272000, China.
  • 5 Department of Hematology, Central Hospital of Baoji, Shaanxi Province, 721008, China. Electronic address: [email protected].
PMID: 31301767 DOI: 10.1016/j.bbrc.2019.06.070
Abstract

Leukemia remains a fatal disease for most patients and effective therapeutic strategies are urgently required. Typhaneoside (TYP) is a major flavonoid in the extract of Pollen Typhae, showing significant biological and pharmacological effects. In the present study, we explored the effects of TYP on acute myeloid leukemia (AML) progression. The results indicated that TYP markedly reduced the cell viability of AML cells and arrested the cell cycle at the G2/M phase by regulating the expression of associated proteins. In addition, TYP significantly induced Apoptosis in AML cells by promoting the activation of Caspase-3. Intracellular and mitochondrial Reactive Oxygen Species (ROS) accumulation were highly detected in AML cells after treatment with TYP. Moreover, TYP clearly induced Ferroptosis in AML cells, and this process was iron-dependent and attendant with mitochondrial dysfunction. We also found that TYP significantly triggered Autophagy in AML cells by promoting the activation of AMP-activated protein kinase (AMPK) signaling, contributing to ferritin degradation, ROS accumulation and ferroptotic cell death ultimately. In conclusion, the findings above provided solid evidences that TYP could be a promising therapeutic agent to prevent AML progression by inducing Apoptosis, ROS production, Autophagy and Ferroptosis.

Keywords

Acute myeloid leukemia (AML); Autophagy; Ferroptosis; ROS accumulation; Typhaneoside (TYP).

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