title: An estrogen receptor alpha-dependent regulation of estrogen receptor-related receptor alpha in the proliferation of endometrial carcinoma cells.
abstract: Estrogen receptor-related receptor alpha (ERRalpha) was reported to compete with estrogen receptor alpha (ERalpha) in a constitutive manner as an orphan nuclear closely related to (ERalpha). To discuss the role of ERRalpha in the endometrial carcinoma cells, this study was performed. ER-responsive endometrial carcinoma cells Ishikawa and ER-nonresponse HEC-1A cells were treated with different concentration of 17beta-E2 or E2 plus ICI 182780. Semiquantitative reverse transcription-polymerase chain reaction and western blot were performed to analysis the expression of human estrogen receptor-related receptor alpha (hERRalpha). Plasmid PLXSN-hERRalpha was constructed and transfected into cells. Selected in the medium containing high-dose G418, the Ishikawa and HEC-1A cells with stable overexpression of hERRalpha were constructed and renamed as Ishikawa/hERRalpha and HEC-1A/hERRalpha, respectively. To discuss the effect of overexpression of hERRalpha in the cell biological behavior (3-[4,5-dimethylth-lazol-2yl]-2,5-diphenyltetrazolium bromid) (MTT) cell assay was performed. Estrogen downregulates ERRalpha expression in ER-positive Ishikawa cells, while upregulates the expression of ERRalpha in ER-negative HEC-1A cells. In Ishikawa cells, the downregulation of 17beta-E2 in ERRalpha expression cells could be blocked by ICI 182780. A decreasing expression of hERalpha was observed in the ER-responsive cells with overexpression of ERRalpha (Ishikawa/hERRalpha). Overexpression of hERRalpha inhibits the cell proliferation in the ERalpha-responsive Ishikawa cells and stimulated the cell proliferation in the ERalpha-nonresponsive HEC-1A cells. Function of hERRalpha depends on the expression and function of hERalpha. ER-mediated signaling might be the important factor resulting in the hormone-dependent endometrial carcinoma, whereas ERRalpha-mediated pathway might act as the vital role in hormone-independent endometrial carcinoma.
authors.affiliation: Department of Obstetrics and Gynecology, Peking University People's Hospital, Beijing, People's Republic of China. dr.sunfengming@gmail.com
authors.forename: P-M
authors.initials: PM
authors.lastname: Sun
authors.forename: M
authors.initials: M
authors.lastname: Gao
authors.forename: L-H
authors.initials: LH
authors.lastname: Wei
authors.forename: A
authors.initials: A
authors.lastname: Mustea
authors.forename: J-L
authors.initials: JL
authors.lastname: Wang
authors.forename: D
authors.initials: D
authors.lastname: Könsgen
authors.forename: W
authors.initials: W
authors.lastname: Lichtenegger
authors.forename: J
authors.initials: J
authors.lastname: Sehouli
mesh_terms: D015153:Blotting, Western; D049109:Cell Proliferation; D016889:Endometrial Neoplasms / Q000378:metabolism*; D047628:Estrogen Receptor alpha / Q000235:genetics* / Q000378:metabolism; D047629:Estrogen Receptor beta / Q000235:genetics / Q000378:metabolism; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D011960:Receptors, Estrogen / Q000378:metabolism*; D014407:Tumor Cells, Cultured; D000097983:ERRalpha Estrogen-Related Receptor
chemical_list: D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D011960:Receptors, Estrogen; D000097983:ERRalpha Estrogen-Related Receptor