Antitumor mechanism of evodiamine, a constituent from Chinese herb Evodiae fructus, in human multiple-drug resistant breast cancer NCI/ADR-RES cells in vitro and in vivo

Carcinogenesis. 2005 May;26(5):968-75. doi: 10.1093/carcin/bgi041. Epub 2005 Feb 10.

Abstract

Drug resistance is one of the main obstacles to the successful treatment of cancer. The availability of agents that are highly effective against drug-resistant cancer cells is therefore essential. The present study was performed to examine the anticancer effects of evodiamine, a major constituent of the Chinese herb Evodiae fructus, in adriamycin-resistant human breast cancer NCI/ADR-RES cells. Evodiamine inhibited the proliferation of NCI/ADR-RES cells in a concentration-dependent manner with a GI50 of 0.59 +/- 0.11 microM. This agent also caused a substantial apoptosis at 1 microM. FACScan flow cytometric analysis of cell cycle progression revealed that a G2/M arrest was initiated after a 12-h exposure to the drug. Evodiamine increased tubulin polymerization as determined by the immunocytochemical and in vivo tubulin polymerization analyses. In a time- and concentration-dependent manner, evodiamine also promoted the phosphorylations of Raf-1 kinase and Bcl-2. The phosphorylation site of Raf-1 kinase was identified to be serine338. The in vivo anticancer effects of evodiamine were evaluated in Balb-c/nude mice following a tumor xenograft implantation of NCI/ADR-RES cells. The antitumor activity of evodiamine against the human multiple-drug resistant tumor xenograft was found to be superior to that of paclitaxel. Evodiamine therefore represents a highly promising chemotherapeutic agent in the treatment of human multiple-drug resistant cancer cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkaloids / pharmacology
  • Animals
  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / metabolism
  • Cell Proliferation / drug effects
  • Drug Resistance, Neoplasm / physiology*
  • Evodia / metabolism*
  • Female
  • Humans
  • Mice
  • Mice, Nude
  • Microtubules / drug effects
  • Paclitaxel / pharmacokinetics
  • Phosphorylation / drug effects
  • Plant Extracts / pharmacology*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-raf / metabolism
  • Quinazolines / pharmacology*
  • Quinolines / pharmacology

Substances

  • Alkaloids
  • Antineoplastic Agents, Phytogenic
  • Gosyuyu
  • Plant Extracts
  • Proto-Oncogene Proteins c-bcl-2
  • Quinazolines
  • Quinolines
  • evodiamine
  • Proto-Oncogene Proteins c-raf
  • Paclitaxel