Progesterone effect on cell growth, ultrastructural aspect and estradiol receptors of normal human breast epithelial (HBE) cells in culture

• Published in: The Journal of steroid biochemistry and molecular biology 2000-06, Vol.73 (3), p.171-181
• Main Authors: Malet, Catherine, Spritzer, Poli, Guillaumin, Delhy, Kuttenn, Frédérique
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Biological and medical sciences; Breast - drug effects; Breast - metabolism; Breast - ultrastructure; Cell Division - drug effects; Cells, Cultured; Epithelial Cells - drug effects; Estradiol; Female; Fundamental and applied biological sciences. Psychology; Humans; Immunohistochemistry; Microscopy, Electron, Scanning; Mother. Fetoplacental unit. Mammary gland. Milk; Normal breast; Pregnancy. Parturition. Lactation; Progesterone; Progesterone - pharmacology; Progesterone Congeners - pharmacology; Progestins; Promegestone - pharmacology; Receptors, Estradiol - metabolism; Vertebrates: reproduction
• ISSN: 0960-0760; 1879-1220
• DOI: 10.1016/S0960-0760(00)00061-3

The stimulating effect of estradiol (E2) on breast cell growth is well documented. However, the actions of progesterone (P) and its derivatives remain controversial. Additional information is therefore necessary. On a culture system of normal human breast epithelial (HBE) cells, we observed an inhibitory effect on cell growth of a long-term P treatment (7 days) in the presence or absence of E2, using two methods: a daily cell count providing a histometric growth index, and [ 3H]-thymidine incorporation during the exponential phase of cell growth. A scanning electron microscopy study confirmed these results. Cells exhibited a proliferative appearance after E2 treatment, and returned to a quiescent appearance when P was added to E2. In both studies, P proved to be as efficient as the synthetic progestin R5020. Moreover, the immunocytochemical study of E2 receptors indicated that E2 increases its own receptor level whereas P and R5020 have the opposite effect, thus limiting the stimulatory effect of E2 on cell growth. In the HBE cell culture system and in long-term treatment, P and R5020 appear predominantly to inhibit cell growth, both in the presence and absence of E2.