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Decursin and decursinol from Angelica gigas inhibit the lung metastasis of murine colon carcinoma

Authors
 Seung Hwa Son  ;  Kwang-Kyun Park  ;  Sun Kyu Park  ;  Young Choong Kim  ;  Yeong Shik Kim  ;  Sang-Kook Lee  ;  Won-Yoon Chung 
Citation
 PHYTOTHERAPY RESEARCH, Vol.25(7) : 959-964, 2011 
Journal Title
PHYTOTHERAPY RESEARCH
ISSN
 0951-418X 
Issue Date
2011
MeSH
Angelica/chemistry* ; Animals ; Antineoplastic Agents, Phytogenic/pharmacology* ; Benzopyrans/pharmacology* ; Butyrates/pharmacology* ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Colonic Neoplasms/pathology* ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors ; LungNeoplasms/drug therapy* ; LungNeoplasms/secondary ; Male ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 9/metabolism ; Mice ; Mice, Inbred BALB C ; NeoplasmMetastasis/drug therapy
Keywords
Keywords: decursin ; decursinol ; Angelica gigas ; colon cancer ; antiinvasive activity ; matrix metalloproteinases
Abstract
The principal objective of the present study was to evaluate the antimetastatic activity of decursin and decursinol isolated from Angelica gigas. Decursin and decursinol inhibited the proliferation and invasion of CT-26 colon carcinoma cells. The expressions of matrix metalloproteinase (MMP)-2 and MMP-9 in cells and the activities in the culture medium were also reduced by decursin and decursinol treatment. In CT-26 cells, the extracellular signal-regulated kinase (ERK) inhibitor inhibited cell proliferation, invasion and MMP-9 expression, and the c-Jun N-terminal kinase (JNK) inhibitor suppressed the expression of both MMPs, as well as cell proliferation and cell invasion. The phosphatidylinositol-3 kinase (PI3K) inhibitor reduced only the expression of MMP-2. In addition, the invasion of CT-26 cells was inhibited by the treatment with anti-MMP-9 antibody, rather than anti-MMP-2 antibody. These results indicate that MMP-9 expression via ERK and JNK plays a critical role for the invasion of CT26 cells. Decursin and decursinol downregulated ERK and JNK phosphorylation. Moreover, oral administration of decursin and decursinol reduced the formation of tumor nodules in the lungs and the increase in lung weight caused by CT-26 metastases. Therefore, both decursin and decursinol may be beneficial antimetastatic agents, targeting MMPs and their upstream signaling molecules.
Full Text
http://onlinelibrary.wiley.com/doi/10.1002/ptr.3372/abstract
DOI
10.1002/ptr.3372
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Park, Kwang Kyun(박광균)
Park, Sun Kyu(박선규)
Son, Seung Hwa(손승화)
Chung, Won Yoon(정원윤) ORCID logo https://orcid.org/0000-0001-8428-9005
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/94245
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