Parker Lynn P, Taylor Douglas D, Kesterson Sarah, Gercel-Taylor Cicek
Division of Gynecologic Oncology, Department of Obstetrics, Gynecology and Women's Health, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Cancer Genomics Proteomics. 2009 May-Jun;6(3):189-94.
Despite optimal primary treatment of ovarian cancer, overall prognosis is poor due to recurrences. While steroid hormone receptors are frequently expressed, the role of estrogen receptor (ER) in ovarian carcinogenesis, response to treatment or prognosis has not been established. We analyzed the gene-expression in response to estradiol (E2) and genistein (Gen) in ovarian cancer cells.
Cell lines (Br-1, UL-1; Oy-1), treated with E2 (10 nM) or Gen (5 microM), were used for gene expression profiling. RT-PCR and Western immunoblotting were used to further analyze gene expression data.
Twenty-four genes were differentially regulated in ovarian cancer cell lines. C3, CLU, COL6A1, DLC1, NME1, NRIP1, PTEN, RAC2, S100A2 were down-regulated with E2 in Br-1 and UL-1 cells. MK167, SERPINB5, SLC7A5, CDK1NA, LCN2, PLAU, PHB2, CTSB, EGLN2, ERBB2, HMGB1, ID2, ITGB4, TOP2A were up-regulated in Oy-1 cells with E2 and/or genistein. ERBB2 and ID2 (E2 and Gen), LCN2, PHB2 and HMGB1 (Gen) were down-regulated in Br-1 cells. ERalpha and ERbeta were detected in all cell lines at different levels.
Variable response of ovarian cancer cells to E2 and Gen was observed. Study of ERs including splice variants, co-regulatory molecules are necessary to understand the relevance of receptors.
