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      Effects of the calciotrophic peptides calcitonin and parathyroid hormone on prostate cancer growth and chemotaxis.

      The Prostate
      Calcitonin, pharmacology, Carcinoma, drug therapy, physiopathology, Cell Division, drug effects, Chemotaxis, Dose-Response Relationship, Drug, Humans, Male, Parathyroid Hormone, Prostatic Neoplasms, Tumor Cells, Cultured

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          Abstract

          The most common site of metastases in prostate cancer is the skeleton and occurs in 70-80% of patients with prostate carcinoma. Calciotrophic peptides are important in the growth and development of normal bone matrix. Three human prostate carcinoma cells lines, DU-145, PC-3, and LNCaP, were exposed to varying concentrations of parathyroid hormone (PTH) or calcitonin (CT). Cell proliferation and chemotaxis were assessed. Proliferation increased in LNCaP cells in a dose-dependent manner following treatment with PTH. Proliferation was not altered in PC-3 cells in response to PTH. Proliferation was decreased in DU-145 and PC-3 cells and increased in LNCaP cells after treatment with CT. Cell chemotaxis was increased in the presence of PTH in DU-145 and PC-3 cells compared to vehicle-treated controls. The combined proliferation and chemotaxis data suggest that PTH has a dual role in prostate carcinoma resulting in an increase in the number and migration of selected prostate cancer cells. With CT, chemotaxis was unchanged in the DU-145 and PC-3 cells and significantly elevated in the LNCaP cell line. The calciotrophic hormones, PTH and CT, may play an integral role in the regulation of prostate cell growth and metastases.

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