文献类型：期刊文献

英文题名：Ganoderic acid T inhibits tumor invasion in vitro and in vivo through inhibition of MMP expression

作者：Chen, Nian-Hong[1,2];Liu, Jian-Wen[2,3];Zhong, Jian-Jiang[1,2]

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

年份：2010

卷号：62

期号：1

起止页码：150

外文期刊名：PHARMACOLOGICAL REPORTS

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000277174500015)】；

基金：Financial support was provided by the Shanghai Science & Technology Commission (project NO. 054319933 and 08DZ1971900) and the Shanghai Leading Academic Discipline Project (project NO. B203 and B505). We would like to thank Dr. B. Vogelstein (Johns Hopkins University, Baltimore, USA) for providing the HCT-116 colon carcinoma cell line. We are also grateful for the technical assistance provided by our fellow workers: Tang Wen and Wang Guan.

语种：英文

外文关键词：ganoderic acid T; metastasis; invasion; MMP-9; uPA

摘要：The traditional Chinese medicinal mushroom, Ganoderma lucidum, has been used in Asia for several thousand years for the prevention and treatment of a variety of diseases, including cancer. In previous work, we purified ganoderic acid T (GA-T) from G. lucidum [28]. In the present study, we investigate the functions of GA-T in terms of its effects on invasion in vitro and metastasis in vivo. A trypan blue dye exclusion assay indicates that GA-T inhibits proliferation of HCT-116 cells, a human colon carcinoma cell line. Cell aggregation and adhesion assays show that GA-T promotes homotypic aggregation and simultaneously inhibits the adhesion of HCT-116 cells to the extracellular matrix (ECM) in a dose-dependent manner. Wound healing assays indicate that GA-T also inhibits the migration of HCT-116 cells in a dose-dependent manner, and it suppresses the migration of 95-D cells, a highly metastatic human lung tumor cell line, in a dose- and time-dependent manner. In addition, GA-T inhibits the nuclear translocation of nuclear factor-kappa B (NF-kappa B) and the degradation of inhibitor of kappa B-alpha (I kappa B alpha), which leads to down-regulated expression of matrix metalloproteinase-9 (MMP-9), inducible nitric oxide synthase (iNOS), and urokinase-type plasminogen activator (uPA). Animal and Lewis Lung Carcinoma (LLC) model experiments demonstrate that GA-T suppresses tumor growth and LLC metastasis and down-regulates MMP-2 and MMP-9 mRNA expression in vivo. Taken together, these results demonstrate that GA-T effectively inhibits cancer cell invasion in vitro and metastasis in vivo, and thus it may act as a potential drug for treating cancer.