Objective: The objective of the study was to determine whether cross-talk occurs between estrogen receptors (ERs) and nuclear factor-kappa-B (NF-kappaB), to assess the functional consequences of such an ER/NF-kappaB interaction, and to identify other unknown regulatory proteins that may participate in the NF-kappaB transcriptional complex.
Study Design: Electromobility gel shifts, reporter gene assays, and mass spectrometry were used to identify proteins interacting with the NF-kappaB deoxyribonucleic acid (DNA) response element.
Results: ER and the p65 subunit of NF-kappaB colocalized on DNA.
Objective: Nuclear factor kappa B (NFkappaB) is a strong anti-apoptotic factor, which is constitutively active in human endometrial cancer cells. Progesterone is the principal growth inhibitory hormone in the endometrial epithelium and promotes apoptosis. To identify the pathways through which progesterone controls NFkappaB function, we explored its genomic and non-genomic effects in endometrial cancer cells.
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