Synergistic antitumour activity of sorafenib in combination with tetrandrine is mediated by reactive oxygen species (ROS)/Akt signaling

Br J Cancer. 2013 Jul 23;109(2):342-50. doi: 10.1038/bjc.2013.334. Epub 2013 Jun 27.

Abstract

Background: Sorafenib is a potent inhibitor against Raf kinase and several receptor tyrosine kinases that has been approved for the clinical treatment of advanced renal and liver cancer. Combining sorafenib with other agents has been shown to improve its antitumour efficacy by not only reducing the toxic side effects but also preventing primary and acquired resistance to sorafenib. We have previously observed that tetrandrine exhibits potent antitumour effects in human hepatocellular carcinoma. In this study, we investigated the synergistic antitumour activity of sorafenib in combination with tetrandrine.

Methods: This was a two-part investigation that included the in vitro effects of sorafenib in combination with tetrandrine on cancer cells and the in vivo antitumour efficacy of this drug combination on tumour xenografts in nude mice.

Results: Combined treatment showed a good synergistic antitumour effect yet spared non-tumourigenic cells. The potential molecular mechanism may be mainly that it activated mitochondrial death pathway and induced caspase-dependent apoptosis in the cancer cells. Accumulation of intracellular reactive oxygen species (ROS) and subsequent activation of Akt may also be involved in apoptosis induction.

Conclusion: The antitumour activity of sorafenib plus tetrandrine may be attributed to the induction of the intrinsic apoptosis pathway through ROS/Akt signaling. This finding provides a novel approach that may broaden the clinical application of sorafenib.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology*
  • Benzylisoquinolines / administration & dosage*
  • Benzylisoquinolines / pharmacology
  • Carcinoma, Hepatocellular / drug therapy*
  • Carcinoma, Hepatocellular / metabolism
  • Carcinoma, Hepatocellular / pathology
  • Drug Synergism
  • HCT116 Cells
  • Humans
  • Liver Neoplasms / drug therapy*
  • Liver Neoplasms / metabolism
  • Liver Neoplasms / pathology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Niacinamide / administration & dosage
  • Niacinamide / analogs & derivatives*
  • Niacinamide / pharmacology
  • Oncogene Protein v-akt / metabolism
  • Oncogene Protein v-akt / physiology
  • Phenylurea Compounds / administration & dosage*
  • Phenylurea Compounds / pharmacology
  • Reactive Oxygen Species / metabolism
  • Reactive Oxygen Species / pharmacology
  • Signal Transduction / drug effects
  • Signal Transduction / physiology
  • Sorafenib
  • Tumor Cells, Cultured
  • Xenograft Model Antitumor Assays

Substances

  • Benzylisoquinolines
  • Phenylurea Compounds
  • Reactive Oxygen Species
  • Niacinamide
  • tetrandrine
  • Sorafenib
  • Oncogene Protein v-akt