[Hormone receptors of target cells of estrogens and relation to cell growth].
Three carcinomatous cell lines have been established in our laboratory and well characterized: two from endometrial carcinoma (MOQ and GUS), one from a pleural effusion of a breast cancer (FAM). These three cell lines have estrogen (ER) and progesterone receptors (PR). A subline of MOQ (MOQ-2) has now lost its receptors and is R-. With this material some paradoxical results have been observed:--estrogens, at physiological concentrations in the culture medium, do not enhance cell proliferation; estrogens are only active in inducing new PR synthesis; but these R+ cells grow in vitro irrespective of the presence of estrogens;--when these cultivated cells are inoculated into nude mice, only FAM (breast cancer cells) grow spontaneously and give a tumor in some animals; MOQ and GUS (endometrial carcinoma) grow only in 20 to 40% of pre-irradiated nude mice; when estrogen-treated, 100% of the mice have a tumour with MOQ without irradiation, 80% a direct tumour with GUS or FAM. This shows that the same cells which are estrogen insensitive in vitro, are estrogen dependent in vivo;--more surprising is the fact that the MOQ-2 cells (ER-) are the most hormono-dependent ones in nude mice and always give rise to a node in mice supplemented with estrogens (100%). These paradoxical results show that, if we know how the estrogens induce protein synthesis in the cell by the ER system, there is still a gap in our understanding of growth promoting activity.