Involvement of Cell Cycle Regulators in Steroid Hormone-Induced Growth of Endometrial Carcinoma

摘要

The involvement of cell cycle regulators in steroid hormone-dependent growth and growth suppression was examined using cultured normal endometrial glandular cells and estrogen receptor (ER)/pregesterone receptor (PR)-positive endometrial carcinoma Ishikawa cells. The results indicated that the estradiol (E2)-induced upregulation of cyclin Dl may play a crucial role in the growth of normal endometrial glandular cells and is mediated by c-Jun via an activating protein (AP)-1-binding site-like sequence of the promoter. However, in ER-positive Ishikawa cells, its molecular mechanism is different from the normal counterpart. In progestin-induced growth suppression, accumulation of p27 protein plays an essential role in both normal and malignant endometrial cells, possibly via inhibition of the ubiqui-tin pathway of p27 degradation.