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

Ya-Sai Sun1, Kiran Thakur1, Fei Hu1

  • 1School of Food and Biological Engineering, Hefei University of Technology, Hefei 230009, PR China.

Pharmacological Research
|December 30, 2019
PubMed

Insights

Icariside II, a compound from Epimedium brevicornum, shows potent anticancer effects against cervical cancer. It inhibits cancer cell growth and triggers cell death, suggesting its potential as a novel therapeutic agent.

Area of Science:

  • Pharmacology
  • Oncology
  • Natural Products

Background:

  • Cervical cancer is a leading cause of cancer-related mortality in women worldwide.
  • There is an ongoing need for novel therapeutic agents to improve cervical cancer treatment outcomes.

Purpose of the Study:

  • To investigate the anticancer activity of Icariside II, a flavonoid from Epimedium brevicornum, against cervical cancer.
  • To elucidate the underlying mechanisms of Icariside II's action on cervical cancer cells.

Main Methods:

  • In vitro studies using Hela cells to assess proliferation inhibition (IC50) and cell cycle arrest.
  • In vivo studies using Hela-originated xenografts in BALB/c nude mice to evaluate tumor growth inhibition.
  • Flow cytometry and immunofluorescence assays to analyze Icariside II-induced cell death pathways.

Main Results:

  • Icariside II significantly inhibited Hela cell proliferation with an IC50 of 9.2 μM and suppressed xenograft tumor growth.
  • Icariside II induced G0/G1 cell cycle arrest by modulating the AKT/Cyclin E/CDK 2 pathway.
  • Icariside II promoted apoptosis via the mitochondria-dependent pathway (Caspase 9/Caspase 3) more effectively than the death receptor pathway (Caspase 8/Caspase 3).

Conclusions:

  • Icariside II demonstrates significant in vitro and in vivo anticancer effects against cervical cancer.
  • The findings support Icariside II as a promising novel therapeutic agent for cervical cancer treatment.

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