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Structure and function of the pS2 gene and estrogen receptor in human breast cancer cells

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Breast Cancer: Cellular and Molecular Biology

Abstract

A significant percentage of breast cancers are estrogen-dependent. These tumors undergo regression when deprived of estrogen or when treated with anti-estrogens [1]. The basis for this hormonal dependence in these cancers is the presence of estrogen receptors (ER). However, the function of the estrogen-receptor complex in promoting the growth of cancer cells is incompletely understood. The MCF-7 cell line, which is derived from a pleural effusion of a human breast cancer [2], contains ER [3] and is dependent on estrogen for optimal growth [4, 5]. In addition, the levels of a variety of mRNAs, proteins and secreted growth factors are under estrogen control in MCF-7 cells [6–10]. As such, these cells represent a good in vitro model system for hormone-dependent human breast cancer. Using these cells we have taken a two-pronged approach to study the molecular basis of estrogen action: 1) the molecular cloning of estrogen-responsive MCF-7 cell gene(s) and 2) the isolation of the human ER cDNA. Of interest is both the function of the gene product of an estrogen-responsive gene and its relationship to cell growth, as well as the mechanism by which estrogen and its receptor control the expression of that gene. We will discuss in this chapter our analysis of one such gene, named pS2, and the polypeptide for which it codes. Included will be a discussion of the localization of the estrogen-responsive DNA element (ERE) to the 5′-flanking region of the pS2 gene.

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© 1988 Kluwer Academic Publishers, Boston/Dordrecht/London

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Stack, G. et al. (1988). Structure and function of the pS2 gene and estrogen receptor in human breast cancer cells. In: Lippman, M.E., Dickson, R.B. (eds) Breast Cancer: Cellular and Molecular Biology. Cancer Treatment and Research, vol 40. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1733-3_8

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  • DOI: https://doi.org/10.1007/978-1-4613-1733-3_8

  • Publisher Name: Springer, Boston, MA

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