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Autocrine Growth Stimulation of the MCF 7 Breast Cancer Cells by the Estrogen-Regulated 52 K Protein^*

Unité d‘Endocrinologie Cellulaire et Moléculaire U 148 INSERM, 34100 Montpellier, France

Address requests for reprints to: Dr. Henri Rochefort, Unite d‘Endocrinologie Cellulaire et Moleculaire, U 148 INSERM, 60, rue de Navacelles, Montpellier 34100, France.

Abstract

The growth of MCF 7 human breast cancer cells is stimulated in vitro by estradiol (E₂) and we have previously shown that estrogen-regulated glycoproteins released into the culture medium can partly mimick this effect.

In this paper, we evaluate the mitogenic activity of the 52 K glycoprotein, which is a major E₂-stimulated protein released by MCF 7 cells. The 52 K protein was purified 600-fold by affinity chromatography on Concahavalin A and an anti-52 K monoclonal antibody Sepharose columns. The 99% purified 52 K protein fraction stimulated the growth of estrogen-deprived MCF 7cells. A mean 1.7-fold increase was obtained with nanomolar concentrations of seven different preparations of 52 K protein. This stimulation represented 40% of the mitogenic effect of E₂. Both the 52 K protein and E₂ induced microvilli at the cell surface but the effect of the 52 K protein ocurred earlier. Other putative growth factors which are also stimulated by E₂ and observed by [³⁵SJcysteine labeling did not comigrate with the purified 52 K protein. Finally, the labeled 52 K protein was found to enter MCF 7 cells and to be processed into an immunoreactive 34 K protein. These data indicate that the E₂-regulated 52 K glycoprotein is an autocrine mitogen on MCF 7 cells in culture and support the hypothesis that estrogens stimulate the growth of mammary cancer via this (and possibly other) secreted protein(s) acting as autocrine (and paracripe?) growth factors. (Endocrinology 118: 1537–1545,1986)

Footnotes

^* This study was supported by INSERM, the Faculte de Medecine de Montpellier, and the Association pour la Recherche sur le Cancer. Part of these results has been presented at the 67th Annual Meeting of The Endocrine Society, Baltimore, MD, 1985 (Abstract 755).

Received June 25, 1985.

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