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[Cancer Research 66, 8648-8654, September 1, 2006]
© 2006 American Association for Cancer Research

Cell, Tumor, and Stem Cell Biology

Type I Collagen Receptor ({alpha}2ß1) Signaling Promotes the Growth of Human Prostate Cancer Cells within the Bone

Christopher L. Hall1, JinLu Dai1, Kenneth L. van Golen2, Evan T. Keller1 and Michael W. Long3

Departments of 1 Urology and 2 Internal Medicine, The University of Michigan; 3 Velcura Therapeutics, Inc., Ann Arbor, Michigan

Requests for reprints: Christopher L. Hall, Department of Urology, University of Michigan, Room 5111 CCGC, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0940. Phone: 734-647-9747; Fax: 734-936-9220; E-mail: clhall{at}umich.edu.

The most frequent site of prostate cancer metastasis is the bone. Adhesion to bone-specific factors may facilitate the selective metastasis of prostate cancer to the skeleton. Therefore, we tested whether prostate cancer bone metastasis is mediated by binding to type I collagen, the most abundant bone protein. We observed that only bone metastatic prostate cancer cells bound collagen I, whereas cells that form only visceral metastases failed to bind collagen. To confirm the relationship between collagen adhesion and bone metastatic potential, a collagen-binding variant of human LNCaP prostate cancer cells was derived through serial passage on type I collagen (LNCaPcol). Fluorescence-activated cell sorting analysis showed that LNCaPcol cells express increased levels of the integrin collagen I receptor {alpha}2ß1 compared with LNCaP cells. Antibodies to the {alpha}2ß1 complex inhibited LNCaPcol binding to collagen, confirming that integrins mediated the attachment. Correspondingly, LNCaPcol cells displayed enhanced chemotactic migration toward collagen I compared with LNCaP cells, an activity that could be blocked with {alpha}2ß1 antibodies. To directly test the role of {alpha}2ß1-dependent collagen binding in bone metastasis, LNCaP and LNCaPcol cells were injected into the tibia of nude mice. After 9 weeks, 7 of 13 (53%) mice injected with LNCaPcol developed bone tumors, whereas 0 of 8 mice injected with LNCaP cells had evidence of boney lesions. LNCaPcol cells were found to express increased levels of the metastasis-promoting RhoC GTPase compared with parental LNCaP. We conclude that collagen I attachment mediated by {alpha}2ß1 initiates motility programs through RhoC and suggest a mechanism for prostate cancer metastasis to the bone. (Cancer Res 2006; 66(17): 8648-54)




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Copyright © 2006 by the American Association for Cancer Research.