期刊
CANCER BIOLOGY & THERAPY
卷 1, 期 3, 页码 300-306出版社
LANDES BIOSCIENCE
DOI: 10.4161/cbt.86
关键词
ovarian cancer; steroid hormones; gonadotropin hormones; cell cycle
类别
资金
- NCI NIH HHS [5P30 CA14089-21, R01 CA 79750, R01 CA 51167] Funding Source: Medline
- NIDDK NIH HHS [R01DK43093] Funding Source: Medline
We examined the effects of the A major female reproductive hormones, estradiol (E2), progesterone (M), follicle stimulating hormone (FSH), and luteinizing hormone (LH) on thymidine incorporation in benign and malignant ovarian epithelial tumors cultured in vitro. Treatment of these tumors with E2, FSH and LH resulted in increased thymidine incorporation while treatment with P4 inhibited growth as well as thymidine incorporation. The inhibitory effect of progesterone could not be reproduced by treating the cells with ligands for other steroid hormone receptors known to interact with P4 such as the mineralocorticoid and glucocorticoid receptors. All cells lines expressed at least the PR-A isoform of the progesterone receptor. ORG2058, R5020, RU486, and ZK98299 acted as progesterone receptor agonists with regard to their effect on thymidine incorporation. P4 down-regulated cyclin B1 expression and cdk1 activity and up-regulated the p21 and p27 proteins. Expression of a reporter gene downstream to an AP-1 responsive element in a plasmid construct transfected into ovarian epithelial tumor cells was induced by P4 and inhibited by RU486. We conclude that P4 inhibits cell cycle activity in ovarian epithelial tumors, in part via down-regulation of the cdk1/cyclin B complex. This inhibitory effect may have therapeutic utility against ovarian epithelial tumors.
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