详细信息
Ganoderic acid Me induces apoptosis through mitochondria dysfunctions in human colon carcinoma cells ( SCI-EXPANDED收录 EI收录)
文献类型:期刊文献
英文题名:Ganoderic acid Me induces apoptosis through mitochondria dysfunctions in human colon carcinoma cells
作者:Zhou, Li[1];Shi, Ping[1];Chen, Nian-Hong[1,2];Zhong, Jian-Jiang[2]
机构:[1]E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]Shanghai Jiao Tong Univ, Key Lab Microbial Metab, Minist Educ, Sch Life Sci & Biotechnol, Shanghai 200240, Peoples R China
年份:2011
卷号:46
期号:1
起止页码:219
外文期刊名:PROCESS BIOCHEMISTRY
收录:;EI(收录号:20105113504823);WOS:【SCI-EXPANDED(收录号:WOS:000286538300030)】;
基金:Financial support from the Shanghai Science and Technology Commission (Project No. 054319933 and 08DZ1971900), the Shanghai Leading Academic Discipline Project (Project No. B203 and B505) and Shanghai Pujiang Program (Project No. 10PJ1402300) is gratefully acknowledged. We thank Prof. B. Vogelstein (Johns Hopkins University Medical Institutions, USA) for generously providing HCT-116 colon carcinoma cell line.
语种:英文
外文关键词:Ganoderic acid Me (GA-Me); p53; Apoptosis; Anti-tumor activity; Traditional Chinese medicine (TCM)
摘要:Ganoderma lucidum, a traditional Chinese medicinal mushroom, has been used in Asia for several thousand years for the prevention and treatment of a variety of diseases including cancer. In our previous work, ganoderic acid Me (GA-Me), as one of bioactive triterpene compounds purified from Ganoderma lucidum, induced p53-mediated sub-G(1) arrest in human colon cells [1]. The apoptotic mechanism of GA-Me induction on tumor cells is yet unclear and was studied in this work. GA-Me was found to possess remarkable cytotoxicity on HCT-116 human colon carcinoma cells in a dose-dependent manner. Interestingly, the expression of anti-tumor protein p53 in GA-Me treated tumor cells was increased in a time dependent manner. Among the pro-apoptotic proteins, Bax was up-regulated, whereas the expression of Bcl-2 was not significantly changed, thus the ratio of Bcl-2/Bax was decreased. Furthermore, GA-Me reduced mitochondria transmembrane potential, released cytochrome c and increased caspase 3 activity during the induced apoptotic process. Our findings show that the anti-cancer bioactivity of GA-Me was mediated by induced apoptosis, resulting from mitochondrial dysfunctions. Our study also suggests that GA-Me may be a novel promising agent for the treatment of human colon carcinoma cells. (C) 2010 Elsevier Ltd. All rights reserved.
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