Cellular and molecular mechanisms of silibinin induces cell-cycle arrest and apoptosis on HeLa cells

Cell Biochem Funct. 2012 Apr;30(3):243-8. doi: 10.1002/cbf.1842. Epub 2011 Dec 13.

Abstract

Silibinin, an effective anti-cancer and chemopreventive agent in various epithelial cancer models, has been reported to inhibit cancer cell growth through mitogenic signalling pathways including cervical cancer. However, the underlying mechanisms are still not well elucidated. Here, we assessed the effect of silibinin on human cervical carcinoma cell cycle modulation, apoptosis induction and associated molecular alterations by employing HeLa cell line. Silibinin treatment of HeLa cells resulted in a G2 arrest and induced a decrease in cyclin-dependent kinases involved in both G1 and G2 progression. In addition, silibinin showed a dose-dependent and a time-dependent apoptotic death in HeLa cells in both the mitochondrial pathway and the death receptor-mediated pathway, providing a strong rationale for future studies evaluating preventive and/or intervention strategies for silibinin in cervical cancer pre-clinical models.

MeSH terms

  • Apoptosis / drug effects*
  • Cell Cycle Checkpoints / drug effects*
  • Cell Proliferation / drug effects
  • Female
  • HeLa Cells
  • Humans
  • Signal Transduction / drug effects
  • Silybin
  • Silymarin / pharmacology*
  • Uterine Cervical Neoplasms / drug therapy
  • Uterine Cervical Neoplasms / metabolism
  • Uterine Cervical Neoplasms / physiopathology*

Substances

  • Silymarin
  • Silybin