2. Academic Validation
  3. Icariside II inhibits tumorigenesis via inhibiting AKT/Cyclin E/ CDK 2 pathway and activating mitochondria-dependent pathway

Icariside II inhibits tumorigenesis via inhibiting AKT/Cyclin E/ CDK 2 pathway and activating mitochondria-dependent pathway

  • Pharmacol Res. 2020 Feb;152:104616. doi: 10.1016/j.phrs.2019.104616.
Ya-Sai Sun 1,  Kiran Thakur 2,  Fei Hu 3,  Jian-Guo Zhang 4,  Zhao-Jun Wei 5
Affiliations

Affiliations

  • 1 School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, PR China. Electronic address: sunyasai@mail.hfut.edu.cn.
  • 2 School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, PR China. Electronic address: kumarikiran@hfut.edu.cn.
  • 3 School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, PR China. Electronic address: hufei@hfut.edu.cn.
  • 4 School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, PR China. Electronic address: zhangjianguo@hfut.edu.cn.
  • 5 School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, PR China. Electronic address: zjwei@hfut.edu.cn.
PMID: 31883767 DOI: 10.1016/j.phrs.2019.104616
Abstract

Cervical Cancer contributes largely in women cancer-related mortality. Herein, Icariside II, a flavonoid extracted from edible and pharmaceutical plant Epimedium brevicornum Maxim, exhibited significant Anticancer activity on cervical Cancer. At first, it was observed that Icariside II inhibited Hela cell proliferation at IC50 (9.2 μM) and the growth of Hela-originated xenografts in BALB/c nude mice. Next, we studied the underlying mechanisms of Icariside II from the aspects of cell growth and cell death. As for cell growth, Icariside II arrested cell cycle at G0/G1 phase through Akt/Cyclin E/CDK 2 from transcriptional and translational levels. As for cell death, Flow Cytometry and Immunofluorescence showed that Icariside II promoted cell death in a dose-dependet manner. And, Icariside II turned to activate the mitochondria-dependent pathway Caspase 9/Caspase 3 much more significantly than death receptor pathway Caspase 8/Caspase 3. Taken together, Icariside II presented Anticancer effect on cervical Cancer both in vitro and in vivo. Our study provides the evidence that Icariside II can be used as a suitable novel agent in cervical Cancer treatment.

Keywords

Apoptosis; Cell cycle arrest; Cervical cancer; Hela cells; Icariside II; Xenografts.

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    ≥98.0%, Caspase-8 Inhibitor