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Antiproliferative Effect of Calcitriol on Human Prostatic Cancer Cell Lines: Unrelated to the Expression of Major Histocompatibility Complex Antigens or Intercellular Adhesion Molecule‐1 (ICAM‐1)
Author(s) -
Yu DaMin,
Tokuda Noriaki,
Naito Seiji,
Yoshikawa Masahiro,
Takahashi Koichi,
Uozumi Jiro,
Kumazawa Joichi
Publication year - 1998
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/j.1442-2042.1998.tb00418.x
Subject(s) - calcitriol , major histocompatibility complex , antigen , flow cytometry , cell culture , calcitriol receptor , microbiology and biotechnology , cell adhesion molecule , human leukocyte antigen , intracellular , receptor , biology , cancer research , immunology , medicine , biochemistry , calcium , genetics
Background: In addition to its role in calcium and phosphorus metabolism, calcitriol (1,25‐dihydroxyvitamin D; 1,25‐D3) demonstrates multiple effects on cell proliferation/differentiation by expressing major histocompatibility complex (MHC) antigens and intercellular adhesion molecule‐1 (ICAM‐1). It has recently been reported that 1,25‐D3 inhibits the growth of prostatic cancer (PCa) cells. In this study we examined the effect of 1,25‐D3 on both the growth and expression of HLA‐ABC, HLA‐DR and ICAM‐1 antigens in PCa cells. Methods: Four human PCa cell lines (PC‐3, PPC‐1, ALVA‐41 and ALVA‐101) were examined. The cell numbers were enumerated, and the effects of interferon‐y (IFN‐y) and 1,25‐D3 on the expression of HLA‐ABC, HLA‐DR and ICAM‐1 were quantitated by flow cytometry. Results: A dose‐dependent antiproliferative effect of 1,25‐D3 was found in all PCa eel Is lines except ALVA‐41. 1,25‐D3 was approximately 10 times as potent as its analogue 24,25‐dihydroxyvitam in D 3 in inhibiting the growth of PC‐3 cells. Also, the relative inhibitory ability of these compounds paralleled the strength of their binding affinities for the 1,25‐D3 receptor, indicating that the antiproliferative effect may require a receptor‐ligand interaction. HLA‐ABC was expressed in PC‐3, ALVA‐41 and ALVA‐101, but not in PPC‐1 cells, while HLA‐DR was not expressed on any of the tested cells. IFN‐y could enhance or induce HLA‐ABC but not HLA‐DR expression in the tested cells. ICAM‐1 was expressed in all cells and slightly up‐regulated by IFN‐y. Conclusion: In this study 1,25‐D3 had an antiproliferative effect on 3 of the 4 examined PCa cell lines.