The effect of anti-oestrogens on cell growth and progesterone receptor concentration in human endometrial cancer cells (Ishikawa)

• Published in: Journal of molecular endocrinology Vol. 6; no. 3; pp. 215 - 221
• Main Authors: JAMIL, A, CROXTALL, J. D, WHITE, J. O
• Format: Journal Article
• Language: English
• Published: Colchester BioScientifica 01.06.1991; Portland Press
• Subjects: Antineoplastic agents; Biological and medical sciences; Cell Division - drug effects; Chemotherapy; Estradiol - analogs & derivatives; Estradiol - pharmacology; Estrogen Antagonists; Female; Humans; Medical sciences; Pharmacology. Drug treatments; Polyunsaturated Alkamides; Receptors, Progesterone - drug effects; Receptors, Progesterone - metabolism; Tamoxifen - analogs & derivatives; Tamoxifen - pharmacology; Tumor Cells, Cultured; Uterine Neoplasms - metabolism; Antineoplastic agent; Human; Cell proliferation; Growth; Estrogen; Malignant tumor; Tamoxifene; Chemotherapy; Cell line; Treatment; Uterus; Female genital system; Antagonist; Sex steroid hormone; Tumor cell; Endometrium; Hormonal receptor
• ISSN: 0952-5041; 1479-6813
• DOI: 10.1677/jme.0.0060215

ASTRACT The effect of two anti-oestrogens, 4-OH tamoxifen and ICI 164,384, on growth and progesterone receptor (PR) concentration was investigated in the endometrial carcinoma cell line, Ishikawa. Growth stimulation in response to 4-OH tamoxifen was antagonized by ICI 164,384, the latter having no agonist effect when used as a single agent. Similarly, ICI 164,384 antagonized oestradiol-stimulated cell growth. PR was significantly increased following treatment with 4-OH tamoxifen, this response being antagonized in the presence of ICI 164,384. Oestradiol increased PR, although to a lesser extent than did 4-OH tamoxifen;the effect of oestradiol on PR was also antagonized by ICI 164,384. Used as a single agent, ICI 164,384 induced a moderate but statistically significant increase in PR, thus demonstrating partial agonist activity. This agonist property of ICI 164,384 may provide a mechanism of maintaining PR, which is down-regulated during conventional progestin therapy, without undesirable mitogenic activity.