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Regulates Estrogen-induced Cell Cycle Progression by Modulating E 2 F 1 Expression *

The I B kinase (IKK) complex consists of the catalytic subunits IKK and IKK and a regulatory subunit, IKK /NEMO. Even though IKK and IKK share significant sequence similarity, they have distinct biological roles. It has been demonstrated that IKKs are involved in regulating the proliferation of both normal and tumor cells, although themechanismsbywhich they function in this process remain to be better defined. In this study, we demonstrate that IKK , but not IKK , is important for estrogen-induced cell cycle progressionby regulating the transcriptionof theE2F1gene as well as other E2F1-responsive genes, including thymidine kinase 1, proliferating cell nuclear antigen, cyclin E, and cdc25A. The role of IKK in regulating E2F1 was not the result of reduced levels of cyclin D1, as overexpression of this gene could not overcome the effects of IKK knock-down. Furthermore, estrogen treatment increased the association of endogenous IKK and E2F1, and this interaction occurred on promoters bound by E2F1. IKK also potentiated the ability of p300/CBP-associated factor to acetylate E2F1. Taken together, these data suggest a novel mechanism by which IKK can influence estrogen-mediated cell cycle progression through its regulation of E2F1.