Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2029428 | Steroids | 2008 | 13 Pages |
Abstract
The purpose of this study was to investigate the role of the oestrogen receptor subtypes ERα and ERβ in mediating the non-genomic effects of 17-β-estradiol (E2) in two human endometrial cancer cell lines (RL95-2 and HEC-1A) expressing different levels of these receptor subtypes. Western blotting analysis using phosphorylation site-specific antibodies showed that physiological concentrations of E2 rapidly (<20 min) activated PKCα, but not PKCδ in the RL95-2 cell line. E2 had no effect on PKCα or PKCδ activity in the HEC-1A cell line and suppressed basal levels of PKA activity in both cell lines. PKCα activation coincided with its membrane translocation. ERα was detected in the RL95-2 cell line by Western blotting and RT-PCR but not in the HEC-1A cells, which did express ERβ. A selective ERα agonist PPT had the same effect as E2 on PKCα activation in the RL95-2 cells, but the selective ERβ agonist DPN had no such effect. A 46 kDa variant of ERα increased in abundance in the cell membrane within 20 min of E2 treatment suggesting that ERα mediated the E2 non-genomic effects on PKCα through the formation of a membrane associated signalling complex.
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Authors
Jian Zhi Yang, Cathal O'Flatharta, Brian J. Harvey, Warren Thomas,