Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (15)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Fenton, J. I.
Right arrow Articles by Hord, N. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fenton, J. I.
Right arrow Articles by Hord, N. G.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis, Vol. 23, No. 6, 1065-1070, June 2002
© 2002 Oxford University Press


CARCINOGENESIS

Membrane-type matrix metalloproteinases mediate curcumin-induced cell migration in non-tumorigenic colon epithelial cells differing in Apc genotype

Jenifer I. Fenton, Margaret S. Wolff, Michael W. Orth1 and Norman G. Hord,2

Department of Food Science and Human Nutrition, Michigan State University, 2110 Anthony Hall East Lansing, MI 48824, USA and
1 Department of Animal Science, Michigan State University, E. Lansing, MI 48824, USA

Colonic epithelial cell migration is required for normal differentiated cell function. This migratory phenotype is dependent upon wild-type adenomatous polyposis coli (Apc) expression. Non-tumorigenic murine colon epithelial cell lines with distinct Apc genotypes, i.e. young adult mouse colon (YAMC; Apc+/+) and immortomouse/Min colon epithelial (IMCE; ApcMin/+ cells) were used to assess the association between the Apc genotype, cell motility and matrix metalloproteinase (MMP) activity. Cells were treated with epidermal growth factor (EGF; 1, 10 and 25 ng/ml), hepatocyte growth factor (HGF; 1, 10 and 25 ng/ml) and/or curcumin (0.1–100 µM). EGF (25 ng/ml) and HGF (25 ng/ml) induced a greater migratory response in YAMC compared with IMCE cells after 24 h (P < 0.05). Treatment with curcumin induced a greater or equivalent migratory response in IMCE than YAMC cells. When migrating cells were treated with Ilomastat® (MMP inhibitor), migration was inhibited in both cell types. High concentrations of Ilomastat® (25 and 50 µM) inhibited migration in both cell types, while low concentrations (10 µM) inhibited HGF-induced IMCE migration. Curcumin-induced migration was inhibited in both cell types at the highest concentration of Ilomastat® (50 µM). Immuno-localization analysis of membrane type-1 (MT1)-MMP indicated that migration is associated with the redistribution of this protein from the endoplasmic reticulum to the plasma membrane. Addition of neutralizing polyclonal antibodies against MT1-MMP or a mixture of MT1, 2- and 3-MMPs demonstrated partial or complete inhibition of cell migration in both cell types, respectively. The data provide the first evidence that migration in non-tumorigenic murine colon epithelial cells is: (i) inducible by EGF and HGF in an Apc genotype-dependent manner, (ii) dependent on MT-MMP activity and (iii) inducible by curcumin in an Apc genotype-independent manner. The data suggest a potential mechanism by which curcumin may induce cells heterozygous for Apc to overcome defective cell migration, a phenotype associated with cell differentiation and apoptosis.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Cancer Prevention ResearchHome page
E. P. Moiseeva and M. M. Manson
Dietary Chemopreventive Phytochemicals: Too Little or Too Much?
Cancer Prevention Research, July 1, 2009; 2(7): 611 - 616.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
J. M. Birmingham, J. V. Busik, F. M. Hansen-Smith, and J. I. Fenton
Novel mechanism for obesity-induced colon cancer progression
Carcinogenesis, April 1, 2009; 30(4): 690 - 697.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
J. I. Fenton, S. D. Hursting, S. N. Perkins, and N. G. Hord
Leptin induces an Apc genotype-associated colon epithelial cell chemokine production pattern associated with macrophage chemotaxis and activation
Carcinogenesis, February 1, 2007; 28(2): 455 - 464.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
J. I. Fenton, S. D. Hursting, S. N. Perkins, and N. G. Hord
Interleukin-6 production induced by leptin treatment promotes cell proliferation in an Apc (Min/+) colon epithelial cell line
Carcinogenesis, July 1, 2006; 27(7): 1507 - 1515.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
J. I. Fenton and N. G. Hord
Stage matters: choosing relevant model systems to address hypotheses in diet and cancer chemoprevention research
Carcinogenesis, May 1, 2006; 27(5): 893 - 902.
[Abstract] [Full Text] [PDF]


Home page
Cancer Epidemiol. Biomarkers Prev.Home page
J. I. Fenton, N. G. Hord, J. A. Lavigne, S. N. Perkins, and S. D. Hursting
Leptin, Insulin-Like Growth Factor-1, and Insulin-Like Growth Factor-2 Are Mitogens in ApcMin/+ but not Apc+/+ Colonic Epithelial Cell Lines
Cancer Epidemiol. Biomarkers Prev., July 1, 2005; 14(7): 1646 - 1652.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
S. A. Lamprecht and M. Lipkin
Migrating colonic crypt epithelial cells: primary targets for transformation
Carcinogenesis, November 1, 2002; 23(11): 1777 - 1780.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.