Breast Cancer Res
Volume 2
Suppl 1 |
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Meeting abstractGrowth inhibition and growth stimulation by estradiol of estrogen receptor transfected human breast epithelial cell lines involve different pathwaysBK Lundholt, P Briand and AE Lykkesfeldt Department of Tumor Endocrinology, Institute of Cancer Biology, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen Ø, Denmark Second International Symposium on the Molecular Biology of Breast Cancer Lillehammer, Norway. 12–16 March 2000 Breast Cancer Res 2000,
2(Suppl 1):P2.02doi:10.1186/bcr151
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2000 Current Science Ltd Full textEpidermal growth factor (EGF) and estradiol (E2) are important mitogens in breast epithelial cells, and expression of epidermal growth factor receptor (EGFR) and estrogen receptor (ER) is often inversely correlated in human breast cancer cells. Stable transfection of ER-negative cells with ER cDNA is not sufficient to restore E2-mediated growth stimulation, suggesting a disturbance of this inverse correlation in ER-transfected cell lines. In this study we used the ER-transfected human breast epithelial cell lines HMT-3522F9, growth inhibited by E2 in the presence of EGF, and HMT-3522F9/S3B, growth stimulated by E2 in the absence of EGF. The E2-mediated growth regulatory differences of the cell lines were not due to altered expression of EGFR, TGFα, or c-erbB2 mRNA. A decreased MAP kinase activity was observed in HMT-3522F9 cells in response to E2, indicating that in these cells altered cross-talk between the ER and the EGFR/MAP kinase signalling pathway could be due to the E2-stimulated growth inhibition. Interestingly, no changes in EGFR, ErbB2 or MAP kinase activity was observed in E2-stimulated in HMT-3522F9/S3B cells in response to E2, suggesting a MAP kinase-independent E2-mediated growth stimulatory mechanism. We are currently investigating the pathway(s) involved in the E2-mediated growth stimulation of HMT-3522F9/S3B cells.
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