Retinoic acid-induced changes in 1 alpha,25-dihydroxyvitamin D3 receptor levels in tumor and nontumor cells derived from rat bone.
The inducibility of 1 alpha,25-dihydroxyvitamin D3 [1,25-(OH)2D3] binding by all-trans-retinoic acid (RA) was examined in tumor-derived clonal bone cell lines, in established clonal cell lines derived from normal embryonic bone, and in cultured bone cell populations freshly isolated from 18- and 21-day fetal and 5-day-old neonatal rat calvaria. Levels of 1,25-(OH)2D3 binding were determined using a single saturating dose (84 pM) of 3H-labeled 1,25-(OH)2D3. Bone-derived tumor cell lines (ROS 17/2.8, ROS 17/2, RCJ 3.2T.1, RCJ 3.2.4.1CAM, RCJ 3.2CE2.1) possessed high basal levels of binding and showed increases in 1,25-(OH)2D3 binding after culture for 24 hours in the presence of 10(-5) M RA. The non-tumor-derived established bone cell lines (RCB 2.2A, RCB 2.2B, RCB 2.2C, RCB 2.2D) showed low basal 1,25-(OH)2D3 binding levels and no change in response to RA, while first subcultures of bone cell populations derived from fetal and neonatal rat calvaria showed decreased 1,25-(OH)2D3 binding, following similar treatment with RA. In representative cell populations, the dose dependency of the RA effect was established. The observed differences in response to RA in the cell lines tested seem to be dependent on whether the cells originated from normal or tumor tissue.[1]References
- Retinoic acid-induced changes in 1 alpha,25-dihydroxyvitamin D3 receptor levels in tumor and nontumor cells derived from rat bone. Petkovich, P.M., Heersche, J.N., Aubin, J.E., Grigoriadis, A.E., Jones, G. J. Natl. Cancer Inst. (1987) [Pubmed]
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