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[Cancer Research 61, 3882-3885, May 15, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Secreted Caveolin-1 Stimulates Cell Survival/Clonal Growth and Contributes to Metastasis in Androgen-insensitive Prostate Cancer1

Salahaldin A. Tahir, Guang Yang, Shin Ebara, Terry L. Timme, Takefumi Satoh, Likun Li, Alexei Goltsov, Michael Ittmann, Joel D. Morrisett and Timothy C. Thompson2

Scott Department of Urology [S. A. T., G. Y., S. E., T. L. T., T. S., L. L., A. G., T. C. T.], Department of Pathology [M. I.], Department of Medicine [K. D. M.], Department of Cell and Molecular Biology [T. C. T.], and Department of Radiology [T. C. T.], Baylor College of Medicine, Houston, Texas 77030, and Veterans Affairs Medical Center [T. L. T., M. I., T. C. T.], Houston, Texas 77030

Caveolin-1 is an integral protein of caveolae, known to play important roles in signal transduction and lipid transport. We demonstrate that caveolin-1 expression is significantly increased in primary and metastatic human prostate cancer after androgen ablation therapy. We also show that caveolin-1 is secreted by androgen-insensitive prostate cancer cells, and that this secretion is regulated by steroid hormones. Significantly, caveolin-1 was detected in the MDL3 fraction of serum specimens from patients with advanced prostate cancer and to a lesser extent in normal subjects. Conditioned media from high passage caveolin-1 secreting, androgen-insensitive, LNCaP cells stimulated increased viability and clonal growth of low passage, caveolin-1-negative, androgen-sensitive, LNCaP cells in vitro, and this effect was blocked by treating the media with caveolin-1 antibody. i.p. injections of caveolin-1 antibody suppressed the orthotopic growth and spontaneous metastasis of highly metastatic, androgen-insensitive caveolin-1-secreting mouse prostate cancer. Overall, our results establish caveolin-1 as an autocrine/paracrine factor that is associated with androgen-insensitive prostate cancer. We demonstrate the potential for caveolin-1 as a therapeutic target for this important malignancy.




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Copyright © 2001 by the American Association for Cancer Research.