Skip Navigation


Carcinogenesis Advance Access originally published online on March 17, 2005
Carcinogenesis 2005 26(5):943-950; doi:10.1093/carcin/bgi070
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
26/5/943    most recent
bgi070v1
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 (12)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Rosette, C.
Right arrow Articles by Denissenko, M. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rosette, C.
Right arrow Articles by Denissenko, M. F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis vol.26 no.5 © Oxford University Press 2005; all rights reserved.

Role of ICAM1 in invasion of human breast cancer cells

Caridad Rosette, Richard B. Roth, Paul Oeth, Andreas Braun, Stefan Kammerer, Jonas Ekblom and Mikhail F. Denissenko *

Sequenom, Inc., San Diego, CA, USA

* To whom correspondence should be addressed Email: mdenissenko{at}sequenom.com

We identified previously a region on chromosome 19p13.2 spanning the genes encoding the intercellular adhesion molecules (ICAM), ICAM1, ICAM4 and ICAM5 as a breast cancer susceptibility locus. Genetic variants in this region were also associated with indicators of disease severity, including higher rates of metastases to other organs. Based on this association, we set out to explore the role of ICAM1 in proliferation and invasion of human breast cancer cells. We observed that ICAM1 downregulation at the mRNA and protein levels led to a strong suppression of human breast cell invasion through a matrigel matrix. Under the same conditions, no significant effect on cell proliferation in vitro was seen. Incubation of cells with an antibody against ICAM1 blocked invasion of the highly metastatic MDA-MB-435 cell line in a dose-dependent manner without affecting cell migration. We also demonstrated that the level of ICAM1 protein expression on the cell surface positively correlated with metastatic potential of five human breast cancer cell lines and that ICAM1 mRNA levels were elevated in breast tumor compared with adjacent normal tissue. These results corroborate our previous genetic finding that variations in the ICAM region are associated with the occurrence of metastases and establish a causal role of ICAM1 in invasion of metastatic human breast carcinoma cell lines.


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
 Exp. Biol. Med.Home page
B. B. Aggarwal, M. E. Van Kuiken, L. H. Iyer, K. B. Harikumar, and B. Sung
Molecular Targets of Nutraceuticals Derived from Dietary Spices: Potential Role in Suppression of Inflammation and Tumorigenesis
Experimental Biology and Medicine, August 1, 2009; 234(8): 825 - 849.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C. J. Clarke, T.-G. Truong, and Y. A. Hannun
Role for Neutral Sphingomyelinase-2 in Tumor Necrosis Factor {alpha}-Stimulated Expression of Vascular Cell Adhesion Molecule-1 (VCAM) and Intercellular Adhesion Molecule-1 (ICAM) in Lung Epithelial Cells: p38 MAPK IS AN UPSTREAM REGULATOR OF nSMase2
J. Biol. Chem., January 12, 2007; 282(2): 1384 - 1396.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
Y.-C. Lin, C.-T. Shun, M.-S. Wu, and C.-C. Chen
A Novel Anticancer Effect of Thalidomide: Inhibition of Intercellular Adhesion Molecule-1-Mediated Cell Invasion and Metastasis through Suppression of Nuclear Factor-{kappa}B
Clin. Cancer Res., December 1, 2006; 12(23): 7165 - 7173.
[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.