Estrogen receptor β and the progression of prostate cancer: role of 5α-andros... - 0 views
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In the prostate, ERβ is highly expressed in the epithelial compartment, where it is the prevailing isoform
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In the gland, DHT may be either reversibly 3α- or irreversibly 3β-hydroxylated by the different 3α- and 3β-hydroxysteroid dehydrogenases respectively (Steckelbroeck et al. 2004); these transformations generate two metabolites respectively 3α-diol and 3β-Adiol, which are both unable to bind the AR. Instead, 3β-Adiol displays a high affinity for ERβ (Kuiper et al. 1998, Nilsson et al. 2001), and it has been proposed that this metabolite may play a key role in prostate development
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ERβ signaling, in contrast to ERα, seems to act as a suppressor of prostate growth, and may be positively involved in breast cancer
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another awesome article dealing with hormone metabolites. Physicians that don't understand metabolites and receptors may be doing more harm than good. One of the mainstays of the treatment of metastatic prostate disease is androgen deprivation therapy. This article requires a reassessment of this due to the DHT metabolite 3-beta androstanediol. This metabolite is produced from DHT production via the enzyme 3beta HSD. This metabolite binds to ER beta, an estrogen receptor, and inhibits proliferation, migration, promotes adhesion (limits spreading), and stimulates apoptosis. This is contrast to 3-alpha androstanediol. Androgen deprivation therapy will decrease 3-beta androstanediol. This is the likely reason for the increased aggressive prostate cancer found in those men using 5 alpha reductase inhibitors.