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[Cancer Research 59, 4453-4457, September 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 4453-4457, September 1, 1999]
© 1999 American Association for Cancer Research

Tumor Biology

Osteonectin Promotes Prostate Cancer Cell Migration and Invasion

A Possible Mechanism for Metastasis to Bone1

Karin Jacob, Mukta Webber, Dafna Benayahu and Hynda K. Kleinman2

Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, NIH, Bethesda, Maryland 20982-4370 [K. J., H. K. K.]; Departments of Zoology and Medicine, Michigan State University, East Lansing, Michigan 48824 [M. W.]; and Department of Cell Biology and Histology, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel [D. B.]

The mechanism underlying the "organ-specific" metastasis of prostate cancer cells to the bone is still poorly understood. It is not clear whether the cells only invade the bone and proliferate there or whether they invade many tissues but survive mainly in the bone ("seed and soil"). Extracts from various organs were used as chemoattractants in the in vitro chemotaxis and invasion assays. Results show that, in comparison with extracts of other tissues, bone extracts promote a 2- to 4-fold increase in chemotaxis by human prostate epithelial cells and a 4-fold increase in the invasive ability of human prostate carcinoma cells. The purified active factor from bone and from marrow stromal-cell-conditioned medium is a low glycosylated osteonectin that specifically promotes the invasive ability of bone-metastasizing prostate (and breast) cancer cells but not that of non-bone-metastasizing tumor cells. It does not stimulate the growth of prostate cancer cells in vitro or in vivo. Because osteonectin specifically enhances matrix metalloprotease activity in prostate and breast cancer cells (and not in other tumor cell types), we conclude that prostate cancer cell metastasis to the bone is, in part, mediated by the ability of osteonectin to promote migration, protease activity, and invasion.




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Copyright © 1999 by the American Association for Cancer Research.