Can someone interpret this post of troubledfinuser2?
RESULTS
1,25(OH)2D3 most substantially increased the expression of the insulin-like growth factor binding protein-3 (IGFBP-3) gene. Our analysis also revealed several novel 1,25(OH)2D3-responsive genes. Interestingly, some of the key genes regulated by 1,25(OH)2D3 are also androgen-responsive genes. 1,25(OH)2D3 also down-regulated genes that mediate androgen catabolism.
CONCLUSIONS
The putative 1,25(OH)2D3 target genes appear to be involved in a variety of cellular functions including growth regulation, differentiation, membrane transport, cell–cell and cell–matrix interactions, DNA repair, and inhibition of metastasis. The up-regulation of IGFBP-3 gene has been shown to be crucial in 1,25(OH)2D3-mediated inhibition of LNCaP cell growth. 1,25(OH)2D3 regulation of androgen-responsive genes as well as genes involved in androgen catabolism suggests that there are interactions between 1,25(OH)2D3 and androgen signaling pathways in LNCaP cells. Further studies on the role of these genes and others in mediating the anti-cancer effects of 1,25(OH)2D3 may lead to better approaches to the prevention and treatment of prostate cancer. © 2004 Wiley-Liss, Inc.
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Real-time RT-PCR showed that DHT at 1–100 nM significantly inhibited 1,25-(OH)2D3-induced expression of 24-hydroxylase in LNCaP cells. Furthermore, the catabolism of 1,25-(OH)2D3 was decreased by 10 nM DHT. An androgen receptor (AR) antagonist, Casodex antagonized the DHT effect, whereas an AR agonist (due to the mutant AR in LNCaP cells) hydroxyflutamide did not.
Since i have not visited the board frequently lately im assuming you have more info on the dht vitamin d3 connection in the prostate. Cant seem to find studies on this site, maybe im just a bad searcher?
If im understanding this right then DHT will lower vitamin d3 and low vitamin d3 initself downregulate genes that mediate androgen breakdown (catabolism)? now what does breakdown (catabolism) in this scenario mean in layman terms?