Abstract:
:In this study we investigated the impact of estrogen antagonists and of 16alpha-OHE1 (an estrogen derivative that binds to and induces transactivation of estrogen receptors) on estrogen metabolism in malignant HepG2 human liver cells featured by high estrogen sulfotransferase (EST); our aim was to clarify the potential correlation of EST and ER. As expected, the HepG2 cells exhibited a very high EST activity, with the majority of estrogen metabolites (over 86%) being detected as sulfates by 24 h. The coincubation of E2 and the antiestrogen tamoxifen induced a weak inhibition of EST activity (from 85.4% to 81.5%), while the coincubation with the pure antagonist ICI-182 and with 16alpha-OHE1 produced a 50% and 90% decrease of EST, respectively. Interestingly, both selective estrogen receptor modulators (SERMs) TAM and ICI-182, along with the same 16alpha-OHE1, gave rise respectively to a 2.8%, 3.2%, and 4.6% of de novo 16alpha-OHE1 formation. The inhibition of EST and the increase of 16alpha-OHE1 formation were both time- and dose-dependent. Our results suggest that EST activity is tightly associated with ER transactivation and can be regulated by selective estrogen receptor modulators (SERMs), including antiestrogens and 16alpha-OHE1. In this framework, 16alpha-OHE1 may have a potential role in human liver carcinogenesis, also through the inhibition of EST and the production of unconjugated, bioavailable estrogens.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Campisi I,Granata OM,Cocciadiferro L,Calabrò M,Polito LM,Carruba Gdoi
10.1111/j.1749-6632.2008.03694.xsubject
Has Abstractpub_date
2009-02-01 00:00:00pages
237-41eissn
0077-8923issn
1749-6632pii
NYAS03694journal_volume
1155pub_type
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