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Ligand structure-dependent differences in activation of estrogen receptor alpha in human HepG2 liver and U2 osteogenic cancer cell lines.

Differences in ligand-activation of estrogen receptor alpha (ER(alpha)) were investigated in human HepG2 liver carcinoma and U2 osteogenic sarcoma cells transfected with wild-type ER (ER-wt) and variants expressing only activation function 1 (ERAF1) or AF2 (ER-AF2). The estrogen-responsive C3-luc construct containing the complement C3 gene promoter linked to a bacterial luciferase reporter gene was used to determine ligand- induced wild-type or variant ER activation. The quality pattern of ER-dependent responses was similar in both cell lines for a series of weakly estrogenic hydroxy and dihydroxyaromatic compounds including p-octylphenol, p-nonylphenol, 2',4',6'-trichloro-4-biphenylol, 2',3',4', 5'-tetrachloro-4-biphenylol, bisphenol A and 2, 2'-bis(p-hydroxyphenyl)-1,1,1-trichloroethane. However, some significant quantitative differences in these compounds were also observed. The weakly estrogenic pesticide, kepone, and the phytoestrogens, resveratrol (a trihydroxystilbene) and naringen (a flavanone), induced distinctly different patterns of responses; induction by these compounds was not observed in either cell line cotransfected with ER-wt or ER-AF2. In contrast, naringen activated ER- AF1 in HepG2 cells and resveratrol activated ER- AF1 in U2 cells. In HepG2 cells cotreated with E2 plus the estrogenic compounds, only BPA and resveratrol exhibited ER(alpha) antagonist activity. Structure-dependent differences in ER(alpha) activation and inhibition are consistent with the increasingly complex patterns of ER action in various tissues and indicate that the estrogenic activity of an individual compound can only be determined by using an extensive testing protocol.[1]

References

  1. Ligand structure-dependent differences in activation of estrogen receptor alpha in human HepG2 liver and U2 osteogenic cancer cell lines. Yoon, K., Pellaroni, L., Ramamoorthy, K., Gaido, K., Safe, S. Mol. Cell. Endocrinol. (2000) [Pubmed]
 
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