文献类型：期刊文献

英文题名：Effects of Ganoderic acid Me on inhibiting multidrug resistance and inducing apoptosis in multidrug resistant colon cancer cells

作者：Jiang, Zijing[1,2];Jin, Tiantian[1,2];Gao, Feng[1,2];Liu, Jianwen[1,2];Zhong, Jianjiang[3];Zhao, Heng[4]

机构：[1]E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]E China Univ Sci & Technol, Sch Pharm, Shanghai 200237, Peoples R China;[3]Shanghai Jiao Tong Univ, Coll Life Sci & Biotechnol, Minist Educ, Key Lab Microbial Metab, Shanghai 200240, Peoples R China;[4]Shanghai Chest Hosp, Dept Thorac Surg, Shanghai 200030, Peoples R China

年份：2011

卷号：46

期号：6

起止页码：1307

外文期刊名：PROCESS BIOCHEMISTRY

收录：;EI(收录号：20111913960751);WOS:【SCI-EXPANDED(收录号:WOS:000291190200013)】；

基金：This work was supported by the National Special Fund for State Key Laboratory of Bioreactor Engineering (Grant No. 2060204), the modernization of Chinese medicine special project for "Shanghai Technology Innovation Action Plan" (Grant No. 08DZ1971900) and the 111 Project (Grant No. B07023), and Shanghai Science and Technology Commission (No. 054319933)was gratefully acknowledged.

语种：英文

外文关键词：Ganoderic acid Me; Multidrug resistance; MDR1; MRPs; Apoptosis

摘要：Ganoderma lucidum is known as a valuable herb in the search for anticancer lead compounds because it has been used for thousands of years as a traditional medication. Triterpenoids are the principal active components in this fungus. Ganoderic acid Me (GA-Me), a pure lanostane triterpene, was isolated from G. lucidum. Our study showed that GA-Me could reverse the multidrug resistance (MDR) in multidrug resistant clone cancer cells. We investigated that GA-Me enhanced the chemosensitivities of anticancer agents in MDR cells. Furthermore. GA-Me inhibited the activity of hMDR1 promoter and this transcriptional suppression was consistent with the inhibitory effect of GA-Me on the mRNA and protein expression level of MDR1. Meanwhile, the expression levels of MRP1 and MRP2 were also inhibited by GA-Me. GA-Me could induce apoptosis in MDR cells via up-regulation of p-p53, p53, Bax, caspase-3, caspase-9 and down-regulation of Bcl-2. In addition, GA-Me stimulated the decline in mitochondrial membrane potential and cytochrome release into cytosol. We concluded that GA-Me could effectively reverse multidrug resistance in MDR colon cancer cells, via repressing expression levels of MDR1, MRPs and regulating apoptosis-related pathways. These results suggested that GA-Me had therapeutic potential against multiclrug resistance as a new agent. (C) 2011 Elsevier Ltd. All rights reserved.