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Phenotypic and Functional Analysis of 1,25-Dihydroxyvitamin D₃ Receptor Mediated Modulation of the Human Myeloma Cell Line RPMI 8226¹

Department of Internal Medicine, Section of Hematology and Oncology, Arizona Health Sciences Center, Tucson, Arizona 85724 [J-F. R., B. G. M. D., T. B.]; Service de Mèdecine B, Hôpital Saint-Eloi, 34059 Montpellier, Cedex, France [J-F. R., C.J.]; Unité Inserm U291, Laboratoire d'Immunopathologie des maladies tumorales et auto-immunes, 34100 Montpellier, Cedex, France [J-F. R., C. D., R. B.], and the Department of Biochemistry, Arizona Health Sciences Center, Tucson, Arizona 85724 [S. L. M., J. W. P., M. R. H.]

Several recent studies have demonstrated the presence of specific receptors for the 1,25-dihydroxyvitamin D₃ (calcitriol) in activated normal lymphocytes. By DNA cellulose chromatography, we show evidence of such specific receptors in the human myeloma cell line RPMI 8226. Nanomolar concentrations of 1,25-dihydroxyvitamin D₃ reduce the proliferation of RPMI 8226 cells significantly and simultaneously induce the appearance of both new properties and phenotype expression, such as butyrate esterase, enhanced expression of CD20 (B1), CD15 (Leu-M1) antigens and chains, and decreased expression of the PC1 antigen using microfluorometric analysis. But such an increased expression of membrane chains was not associated with an enhanced secretion of chains. Furthermore, the bone resorbing activity produced normally by RPMI 8226 cells was reduced significantly after 1,25-dihydroxyvitamin D₃ treatment. The possible mechanisms and significance of these new functional and phenotypic properties are discussed with respect to the B-cell lineage.

¹ This work was supported by grants from l'Association pour la Recherche sur le Cancer (Paris, France), the Philippe Foundation, and Grants CA 17904, AM 15781, and AM 33351 from NIH, Bethesda, MD.

² To whom requests for reprints should be addressed, at Unité Inserm U291, 99, rue Puech Villa-Zolad, 34100 Montpellier, Cédex, France.

Received 6/10/87. Revised 11/11/87. Accepted 12/ 4/87.