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Epidermal growth factor (EGF) receptors are present in human breast cancer and probably mediate the effects of EGF and the autocrine effects of alpha-transforming growth factors, produced by breast cancer cells. Steroid hormones influence the growth of some human cancers, and both direct and indirect effects on cell proliferation have been proposed. One potential indirect effect of steroids would be to augment sensitivity to other endocrine and autocrine factors by up-regulation of their receptors. We therefore investigated the effects of various steroids on EGF receptor expression in T-47D, MCF-7, and BT 20 human mammary carcinoma cells in culture. Preincubation of T-47D cells for 24 h with a series of androgens, estrogens, glucocorticoids, and progestins resulted in a significant enhancement of specific 125I-EGF binding in the presence of progestins only. Increased binding of EGF was associated with neither a change in cell number nor changes in the specific binding of concanavalin A, insulin, or calcitonin but was accompanied by an increase in lactogenic receptor expression. When assayed at 20 degrees C, increased EGF binding was due to an increase in receptor number (33,380 +/- 7,410 sites/cell in control cultures; 67,460 +/- 20,330 sites/cell in cultures treated with 1 nM medroxyprogesterone acetate for 24 h; P less than 0.05) without a change in receptor affinity. Two- to 3-fold increases in receptor number were also apparent when binding was measured at 4 degrees C, indicating that the effect was due to an increase in expression of receptor at the cell surface rather than progestin effects on internalization and degradation. These data illustrate that the expression of EGF receptor in some breast cancer cells is regulated in part by mechanisms mediated via the progesterone receptor, since the effect was confined to progestins, potency among a series of progestins was correlated with their affinities for progesterone receptor, and sensitivity among the three cell lines studied was related to the presence and concentration of cellular progesterone receptor.
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
February 1986,
Proceedings of the National Academy of Sciences of the United States of America,
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
January 2000,
The Journal of clinical endocrinology and metabolism,
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
November 1991,
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research,
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
March 1988,
Cancer research,
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
January 1997,
Cancer detection and prevention,
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
May 1992,
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research,
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
December 2012,
The journal of obstetrics and gynaecology research,
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
October 1982,
The Journal of biological chemistry,
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
February 1999,
Clinical cancer research : an official journal of the American Association for Cancer Research,
L J Murphy, and
R L Sutherland, and
B Stead, and
L C Murphy, and
L Lazarus
April 1988,
The Journal of biological chemistry,
