Carcinogenesis Advance Access published online on November 17, 2006
Carcinogenesis, doi:10.1093/carcin/bgl217
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Pathology, Catholic University of Daegu School of Medicine, Daegu 705-718, Korea
* To whom correspondence should be addressed. The expression of matrix metalloproteinase-9 (MMP-9) has been implicated in the invasion and metastasis of cancer cells. Here we found that an antitumor antibiotic, ascofuranone, inhibits invasion and MMP-9 induction induced by phorbol myristate acetate (PMA) in human cell lines. Ascofuranone also inhibits the protein expression and transcription of MMP-9 induced by tumor necrosis factor-
Received July 10, 2006
Revised October 9, 2006
Accepted November 2, 2006
CARCINOGENESIS
Ascofuranone Suppresses PMA-mediated matrix metalloproteinase-9 gene activation through the Ras/Raf/MEK/ERK and Ap1-dependent mechanisms
Hyun-Ji Cho 1, Jeong Han Kang 1, Jong-Young Kwak 2, Tae-Sung Lee 3, In-Seon Lee 4, Nam-Gyu Park 5, Hiroo Nakajima 6, Junji Magae 7, and Young-Chae Chang 1 *
2 Medical Research Center (MRC) for Cancer Molecular Therapy, Dong-A University, Busan, Korea
3 Department of Obstetrics and Gynecology, Catholic University of Daegu School of Medicine, Daegu 705-718, Korea
4 The Center for Traditional Microorganism Resources (TMR), Keimyung University, Daegu 704-701, Korea
5 Department of Biotechnology and Bioengineering and Bioengineering, Pukyong National University, Busan 608-737, Korea
6 Department of Endocrine, Breast Surgery, Kyoto Prefectural University of Medicine, Kyoto, 602-0841, Japan
7 Department of Biotechnology, Institute of Research and Innovation, 1201 Takada, Kashiwa 277-0861, Japan
Young-Chae Chang, E-mail: ycchang{at}cu.ac.kr
![]()
Abstract
. The inhibition of MMP-9 induction was observed in human cancer cell lines as well as primary rat mesangial cells. Furthermore, as evidenced by MMP-9 promoter and electrophoretic mobility shift assays, ascofuranone specifically inhibited MMP-9 gene expression by blocking PMA-stimulated activation of activator protein-1 (AP-1). In addition, ascofuranone suppressed PMA-induced phosphorylation of Ras, Raf, MEK and ERK, upstream factors involved in AP-1activation, while the phosphorylation of p38 and JNK/MAPK was not affected by ascofuranone, suggesting that the primary target of ascofuranone for suppression of the AP-1 inudction is present in upstream of ERK signaling pathway. These results suggest that the suppression of MMP-9 expression, at least in part, contributes to the anti-tumor activity of ascofuranone.![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
P. Montreekachon, P. Chotjumlong, V. Reutrakul, and S. Krisanaprakornkit Involvement of Cytosolic Phospholipase A2{alpha} in MMP-9 Up-regulation Journal of Dental Research, November 1, 2009; 88(11): 1031 - 1036. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. K. Park, Y. S. Hwang, K.-K. Park, H.-J. Park, J. Y. Seo, and W.-Y. Chung Kalopanaxsaponin A inhibits PMA-induced invasion by reducing matrix metalloproteinase-9 via PI3K/Akt- and PKC{delta}-mediated signaling in MCF-7 human breast cancer cells Carcinogenesis, July 1, 2009; 30(7): 1225 - 1233. [Abstract] [Full Text] [PDF] |
||||
![]() |
M.-H. Pan, Y.-S. Chiou, W.-J. Chen, J.-M. Wang, V. Badmaev, and C.-T. Ho Pterostilbene inhibited tumor invasion via suppressing multiple signal transduction pathways in human hepatocellular carcinoma cells Carcinogenesis, July 1, 2009; 30(7): 1234 - 1242. [Abstract] [Full Text] [PDF] |
||||
![]() |
C.-W. Lin, W.-C. Hou, S.-C. Shen, S.-H. Juan, C.-H. Ko, L.-M. Wang, and Y.-C. Chen Quercetin inhibition of tumor invasion via suppressing PKC{delta}/ERK/AP-1-dependent matrix metalloproteinase-9 activation in breast carcinoma cells Carcinogenesis, September 1, 2008; 29(9): 1807 - 1815. [Abstract] [Full Text] [PDF] |
||||
![]() |
S.-O. Lee, Y.-C. Chang, K. Whang, C.-H. Kim, and I.-S. Lee Role of NAD(P)H:quinone oxidoreductase 1 on tumor necrosis factor-{alpha}-induced migration of human vascular smooth muscle cells Cardiovasc Res, November 1, 2007; 76(2): 331 - 339. [Abstract] [Full Text] [PDF] |
||||


