le-135 and Prostatic-Neoplasms
le-135 has been researched along with Prostatic-Neoplasms* in 1 studies
Other Studies
1 other study(ies) available for le-135 and Prostatic-Neoplasms
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Retinoic acid via RARalpha inhibits the expression of 24-hydroxylase in human prostate stromal cells.
25-Hydroxyvitamin D(3)-24-hydroxylase (24-hydroxylase) is an important inactivating enzyme and its expression is induced by 25-hydroxyvitamin D3 (25OHD3) and 1alpha,25-dihydroxyvitamin D3 (1alpha,25-(OH)2D3) through action of heterodimers of vitamin D receptor (VDR) and retinoid X receptor (RXR). RXRs also act as heterodimer partners for retinoic acid receptors (RARs), mediating the action of all-trans-retinoic acid (ATRA). Prostate stroma plays a crucial role in prostate cancer development and benign prostatic hyperplasia. We demonstrate here that ATRA markedly reduced the expression of 24-hydroxylase mRNA induced by 25OHD3 and 1alpha,25-(OH)2D3 in human prostatic stromal cells P29SN and P32S but not in epithelial cells PrEC or cancer cells LNCaP. By using transfection and RAR-selective ligands, we found that the inhibitory effect of ATRA on 24-hydroxylase expression in stromal cells was mediated by RARalpha but not by RARbeta. Moreover, the ATRA-induced expression of RARbeta was also mediated by RARalpha. The combined treatment of 1alpha,25-(OH)2D3 and RARalpha agonist Am80 at 10 nM exhibited strong growth-inhibitory effect whereas either alone had no effect. Our data suggest that ATRA suppresses 24-hydroxylase expression through RARalpha-dependent signaling pathway and can enhance vitamin D action in suppression of cell growth. Topics: Benzoates; Calcitriol; Cell Line; Cell Line, Tumor; Cells, Cultured; Dibenzazepines; Epithelial Cells; Gene Expression Regulation; Humans; Male; Prostate; Prostatic Neoplasms; Receptors, Retinoic Acid; Retinoic Acid Receptor alpha; Retinoid X Receptors; Retinoids; Steroid Hydroxylases; Tetrahydronaphthalenes; Transfection; Tretinoin; Vitamin D3 24-Hydroxylase | 2005 |