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.
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Authors | Wan-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 |
Journal | Bioorganic & medicinal chemistry letters
(Bioorg Med Chem Lett)
Vol. 20
Issue 20
Pg. 6145-8
(Oct 15 2010)
ISSN: 1464-3405 [Electronic] England |
PMID | 20817519
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2010 Elsevier Ltd. All rights reserved. |
Chemical References |
- Antineoplastic Agents
- Triterpenes
- bcl-2-Associated X Protein
- methyl antcinate A
- Caspase 3
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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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