This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Iiizumi, M. Articles by Watabe, K. Search for Related Content PubMed PubMed Citation Articles by Iiizumi, M. Articles by Watabe, K. Related Collections Tumor Biology Tumor Biology: Invasion and Metastasis

Interaction of Duffy Antigen Receptor for Chemokines and KAI1: A Critical Step in Metastasis Suppression

Department of Medical Microbiology and Immunology, Southern Illinois University School of Medicine, Springfield, Illinois

Requests for reprints: Kounosuke Watabe, Department of Medical Microbiology and Immunology, Southern Illinois University School of Medicine, 801 North Rutledge Street, P.O. Box 19626, Springfield, IL 62794-9626. Phone: 217-545-3969; Fax: 217-545-3227; E-mail: kwatabe{at}siumed.edu.

Tumor metastases suppressor protein KAI1/CD82 is capable of blocking the tumor metastases without affecting the primary tumor formation, and its expression is significantly down-regulated in many types of human cancers. However, the exact molecular mechanism of the suppressor function of KAI1 remains elusive. Evidence from our laboratory supports a model in which tumor cells dislodge from the primary tumor and intravasate into the blood or lymphatic vessels followed by attachment to the endothelial cell surface whereby KAI1 interacts with the Duffy antigen receptor for chemokines (DARC) protein. This interaction transmits a senescent signal to cancer cells expressing KAI1, whereas cells that lost KAI1 expression can proliferate, potentially giving rise to metastases. Our model of the mechanism of action of KAI1 shows that metastasis suppressor activity can be dependent on interaction with host tissue and explains how KAI1 suppresses metastasis without affecting primary tumor formation. Taken together, in vitro and in vivo studies identify the KAI1-DARC interaction as a potential target for cancer therapy. [Cancer Res 2007;67(4):1411–4]

This article has been cited by other articles:

				T. Lotan, J. Hickson, J. Souris, D. Huo, J. Taylor, T. Li, K. Otto, S. D. Yamada, K. Macleod, and C. W. Rinker-Schaeffer c-Jun NH2-Terminal Kinase Activating Kinase 1/Mitogen-Activated Protein Kinase Kinase 4-Mediated Inhibition of SKOV3ip.1 Ovarian Cancer Metastasis Involves Growth Arrest and p21 Up-regulation Cancer Res., April 1, 2008; 68(7): 2166 - 2175. [Abstract] [Full Text] [PDF]