Silibinin inhibits the invasion of human lung cancer cells via decreased productions of urokinase-plasminogen activator and matrix metalloproteinase-2

doi:10.1002/mc.20018

中山醫學大學機構典藏 CSMUIR > 醫學院 > 生化微生物免疫研究所 > 期刊論文 > Item 310902500/11530

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/11530

Title:	Silibinin inhibits the invasion of human lung cancer cells via decreased productions of urokinase-plasminogen activator and matrix metalloproteinase-2
Authors:	Chu, Shu-Chen Chiou, Hui-Ling Chen, Pei-Ni Yang, Shun-Fa Hsieh, Yih-Shou
Contributors:	中山醫學大學
Keywords:	silibinin;MMP-2;u-PA;TIMP-2
Date:	2004
Issue Date:	2015-07-22T05:23:41Z (UTC)
ISSN:	0899-1987
Abstract:	Cancer metastasis, involving multiple processes and various cytophysiological changes, is a primary cause of cancer death and may complicate the clinical management, even lead to death. Silibinin is a flavonoid antioxidant and wildly used for its antihepatotoxic properties and recent studies have revealed pleiotropic anticancer and antiproliferative capabilities of silibinin. In this study, we first observed that silibinin exerted a dose- and time-dependent inhibitory effect on the invasion and motility, but hardly on the adhesion, of highly metastatic A549 cells in the absence of cytotoxicity. To look at the precise involvement of silibinin in cancer metastasis, A549 cells were treated with silibinin at various concentrations, up to 100 μM, for a defined period and then subjected to gelatin zymography, casein zymography and Western blot to investigate the impacts of silibinin on metalloproteinase-2 (MMP-2), urokinase plasminogen activator (u-PA), and tissue inhibitor of metalloproteinase-2 (TIMP-2), respectively. The results showed that a silibinin treatment may decrease the expressions of MMP-2 and u-PA in a concentration- and time-dependent manner and enhance the expression of TIMP-2. Further analysis with semi-quantitative RT-PCR showed that silibinin may regulate the expressions of MMP-2 and u-PA on the transcriptional level while on the translational or post-translational level for TIMP-2. © 2004 Wiley-Liss, Inc.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11530 http://dx.doi.org/10.1002/mc.20018
Relation:	Molecular Carcinogenesis Volume 40, Issue 3, pages 143–149, July 2004
Appears in Collections:	[生化微生物免疫研究所] 期刊論文

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