Abstract
The human breast cancer cell line MCF-7 requires oestrogen to produce and promote growth of tumours in athymic mice. in vitro, however, MCF-7 cells proliferate rapidly without supply of oestrogen (Briand & Lykkesfeldt, 1984). Oestrogen stimulation of proliferation of MCF-7 cells can be achieved when the cells are grown at high concentration of newborn calf serum (NCS, 10%) or oestrogen deprived foetal calf serum (10%). The stimulation involves an abolishment of inhibitory activity present in the serum. The oestradiol stimulated cultures grow rapidly for a much longer time period and attain a much higher cell density than the unstimulated cultures. Oestrogen is specific for the promotion of cell proliferation and only oestrogen receptor positive cell lines with a functional oestrogen receptor mechanism can be stimulated. We assume that oestradiol acts directly on the cells and via the oestrogen receptor mechanism induces the synthesis of a substance which abolishes the inhibitory activity in serum. We call this mechanism of action an indirect stimulation of cell proliferation. A similar mechanism may exist in vivo since we find that serum from athymic mice contains a growth inhibitory activity towards MCF-7 cells and the inhibitory effect can be abolished by oestradiol.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 24 print issues and online access
$259.00 per year
only $10.79 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
Rights and permissions
About this article
Cite this article
Lykkesfeldt, A., Briand, P. Indirect mechanism of oestradiol stimulation of cell proliferation of human breast cancer cell lines. Br J Cancer 53, 29–35 (1986). https://doi.org/10.1038/bjc.1986.5
Issue Date:
DOI: https://doi.org/10.1038/bjc.1986.5
This article is cited by
-
MCM3 upregulation confers endocrine resistance in breast cancer and is a predictive marker of diminished tamoxifen benefit
npj Breast Cancer (2021)
-
A suppressive role of guanine nucleotide-binding protein subunit beta-4 inhibited by DNA methylation in the growth of anti-estrogen resistant breast cancer cells
BMC Cancer (2018)
-
Gene expression profiling identifies FYN as an important molecule in tamoxifen resistance and a predictor of early recurrence in patients treated with endocrine therapy
Oncogene (2015)
-
Integrative analyses of gene expression and DNA methylation profiles in breast cancer cell line models of tamoxifen-resistance indicate a potential role of cells with stem-like properties
Breast Cancer Research (2013)
-
Targeting of the adaptor protein Tab2 as a novel approach to revert tamoxifen resistance in breast cancer cells
Oncogene (2012)