Skip Navigation


Carcinogenesis Advance Access originally published online on February 10, 2005
Carcinogenesis 2005 26(5):968-975; doi:10.1093/carcin/bgi041
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Material
Right arrow All Versions of this Article:
26/5/968    most recent
bgi041v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (12)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Liao, C.-H.
Right arrow Articles by Teng, C.-M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liao, C.-H.
Right arrow Articles by Teng, C.-M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis vol.26 no.5 © Oxford University Press 2005; all rights reserved.

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

Cho-Hwa Liao 1, Shiow-Lin Pan 1, Jih-Hwa Guh 2, Ya-Ling Chang 1, Hui-Chen Pai 1, Chun-Hung Lin 1 and Che-Ming Teng 1, *

1 Pharmacological Institute and 2 School of Pharmacy, College of Medicine, National Taiwan University, Taipei 100, Taiwan

* To whom correspondence should be addressed at: Room 1143, No. 1, Jen-Ai Road, Sec. 1, Pharmacological Institute, College of Medicine, National Taiwan University, Taipei 100, Taiwan. Tel/Fax: +886-2-2322-1742; Email: cmteng{at}ntumc.org

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 µM. This agent also caused a substantial apoptosis at 1 µM. 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.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Molecular Cancer TherapeuticsHome page
T.-J. Lee, E. J. Kim, S. Kim, E. M. Jung, J.-W. Park, S. H. Jeong, S. E. Park, Y. H. Yoo, and T. K. Kwon
Caspase-dependent and caspase-independent apoptosis induced by evodiamine in human leukemic U937 cells.
Mol. Cancer Ther., September 1, 2006; 5(9): 2398 - 2407.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.