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Methylantcinate A induces tumor specific growth inhibition in oral cancer cells via Bax-mediated mitochondrial apoptotic pathway.

Abstract
An ergostane type triterpenoid methylantcinate A (MAA) isolated from the fruiting bodies of Antrodia camphorata inhibited the growth of oral cancer cell lines OEC-M1 and OC-2 in a dose-dependent manner, without cytotoxic to normal oral gingival fibroblast cells. The major mechanism of growth inhibition was apoptosis induction, as shown by flow cytometric analysis of annexin V-FITC and propidium iodide staining, caspase-3 activation and DNA fragmentation. The increased expression of pro-apoptotic Bax, poly-(ADP-ribose) polymerase cleavage, and activated caspase-3 and decreased expression of anti-apoptotic Bcl-2 and Bcl-xL were also observed. These results provide the first evidence that the anti-oral cancer effects of MAA may involve a mechanism through the mitochondrial dependent pathway. Thus, results reported here may offer further impulse to the development of MAA analogues as potential chemotherapeutic targets for oral cancer complications.
AuthorsWan-Chi Tsai, Yerra Koteswara Rao, Shih-Shen Lin, Ming-Yung Chou, Yi-Ting Shen, Chih-Hao Wu, Madamanchi Geethangili, Chi-Chiang Yang, Yew-Min Tzeng
JournalBioorganic & medicinal chemistry letters (Bioorg Med Chem Lett) Vol. 20 Issue 20 Pg. 6145-8 (Oct 15 2010) ISSN: 1464-3405 [Electronic] England
PMID20817519 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2010 Elsevier Ltd. All rights reserved.
Chemical References
  • Antineoplastic Agents
  • Triterpenes
  • bcl-2-Associated X Protein
  • methyl antcinate A
  • Caspase 3
Topics
  • Antineoplastic Agents (isolation & purification, pharmacology)
  • Antrodia (chemistry)
  • Apoptosis (drug effects)
  • Caspase 3 (metabolism)
  • Cell Line
  • Cell Line, Tumor
  • Fibroblasts (drug effects)
  • Fruiting Bodies, Fungal (chemistry)
  • Gene Expression Regulation, Neoplastic (drug effects)
  • Humans
  • Mitochondria (drug effects)
  • Mouth Neoplasms (drug therapy)
  • Triterpenes (isolation & purification, pharmacology)
  • Up-Regulation (drug effects)
  • bcl-2-Associated X Protein (genetics, metabolism)

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