Dehydroepiandrosterone-induces miR-21 transcription in HepG2 cells through estrogen receptor β and androgen receptor.
作者： Yun Teng , Lacey M. Litchfield , Margarita M. Ivanova , Russell A. Prough , Barbara J. Clark
DOI: 10.1016/J.MCE.2014.05.007
关键词: Androgen receptor 、 Dihydrotestosterone 、 Androgen 、 Estrogen receptor 、 Dehydroepiandrosterone 、 Estrogen receptor beta 、 Biology 、 Downregulation and upregulation 、 Cell growth 、 Internal medicine 、 Endocrinology
摘要: Although oncomiR miR-21 is highly expressed in liver and overexpressed hepatocellular carcinoma (HCC), its regulation uncharacterized. We examined the effect of physiologically relevant nanomolar concentrations dehydroepiandrosterone (DHEA) DHEA sulfate (DHEA-S) on expression HepG2 human hepatoma cells. 10nM DHEA-S increase pri-miR-21 transcription Dietary increased vivo mouse liver. siRNA inhibitor studies suggest that requires desulfation for activity DHEA-induced involves metabolism to androgen estrogen receptor (AR ER) ligands. Activation ERβ AR by metabolites androst-5-ene-3,17-dione (ADIONE), androst-5-ene-3β,17β-diol (ADIOL), dihydrotestosterone (DHT), 5α-androstane-3β,17β-diol (3β-Adiol) transcription. cell proliferation decreased Pdcd4 protein, a bona fide miR-21. Estradiol (E2) inhibited via ERα. recruitment promoter within VMP1/TMEM49 gene, with possible significance carcinoma.
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