receptor activated ca2+ release is inhibited by boric acid in prostate cancer cells受体激活钙离子释放抑制前列腺癌细胞的硼酸.pdfVIP

Receptor Activated Ca2+ Release Is Inhibited by Boric Acid in Prostate Cancer Cells 1 2 1 1,3 Kimberly Henderson , Salvatore L. Stella, Jr. , Sarah Kobylewski , Curtis D. Eckhert * 1 Molecular Toxicology, School of Public Health, University of California Los Angeles, Los Angeles, California, United States of America, 2 Neurobiology, Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America, 3 Environmental Health Sciences, School of Public Health, University of California Los Angeles, Los Angeles, California, United States of America Abstract Background: The global disparity in cancer incidence remains a major public health problem. We focused on prostate cancer since microscopic disease in men is common, but the incidence of clinical disease varies more than 100 fold worldwide. Ca2+ signaling is a central regulator of cell proliferation, but has received little attention in cancer prevention. We and others have reported a strong dose-dependent reduction in the incidence of prostate and lung cancer within populations exposed to boron (B) in drinking water and food; and in tumor and cell proliferation in animal and cell culture models. Methods/Principal Findings: We examined the impact of B on Ca2+ stores using cancer and non-cancer human prostate cell lines, Ca2+ indicators Rhod-2 AM and Indo-1 AM and confocal microscopy. In DU-145 cells, inhibition of Ca2+ release was apparent following treatment with Ringers containing RyR agonists cADPR, 4CmC or caffeine and respective levels of BA (50 mM), (1, 10 mM) or