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Endocrinology Vol. 141, No. 1 10-17
Copyright © 2000 by The Endocrine Society

ARTICLES

Calcitriol-Induced Apoptosis in LNCaP Cells Is Blocked By Overexpression of Bcl-21

Sarah E. Blutt, Timothy J. McDonnell, Tara C. Polek and Nancy L. Weigel

Department of Molecular and Cellular Biology (S.E.B., T.C.P., N.L.W.), Baylor College of Medicine, Houston, Texas 77030; Department of Molecular Pathology (T.J.M.), The University of Texas, M.D. Anderson Cancer Center, Houston, Texas 77030

Address all correspondence and requests for reprints to: Dr. Nancy L. Weigel, Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030. E-mail: nweigel{at}bcm.tmc.edu

While the role of vitamin D in bone and mineral metabolism has been investigated extensively, the role of the vitamin D receptor in other tissues is less well understood. 1,25-dihydroxyvitamin D3 (calcitriol) can act as a differentiating agent in normal tissues and can inhibit the growth of many cancer cell lines including LNCaP prostate cancer cells. We have shown previously that calcitriol causes LNCaP cell accumulation in the G0/G1 phase of the cell cycle. In this study, we demonstrate that calcitriol also induces apoptosis of LNCaP cells. The calcitriol-induced apoptosis is accompanied by a down-regulation of Bcl-2 and Bcl-XL proteins, both of which protect cells from undergoing apoptosis. Other proteins important in apoptotic control, Bax, Mcl-1, and Bcl-Xs, are unaffected by calcitriol treatment. We find that overexpression of Bcl-2 blocks calcitriol-induced apoptosis and reduces, but does not eliminate, calcitriol-induced growth inhibition. We conclude that both regulation of cell cycle and the apoptotic pathway are involved in calcitriol action in prostate cancer cells.




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