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

doi:10.1016/j.bmcl.2010.08.006

中山醫學大學機構典藏 CSMUIR > 醫學科技學院 > 醫學檢驗暨生物技術學系暨碩士班 > 期刊論文 > Item 310902500/11807

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11807

Title:	Methylantcinate A induces tumor specific growth inhibition in oral cancer cells via Bax-mediated mitochondrial apoptotic pathway.
Authors:	Tsai, WC Rao, YK Lin, SS Chou, MY Shen, YT Wu, CH Geethangili, M Yang, CC Tzeng, YM
Contributors:	中山醫學大學
Date:	2010
Issue Date:	2015-07-29T08:54:33Z (UTC)
ISSN:	0960-894X
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. Copyright © 2010 Elsevier Ltd. All rights reserved.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11807 http://dx.doi.org/10.1016/j.bmcl.2010.08.006
Relation:	Bioorg Med Chem Lett. 2010 Oct 15;20(20):6145-8.
Appears in Collections:	[醫學檢驗暨生物技術學系暨碩士班] 期刊論文

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