BRCA2 is closely related to the pathogenesis of breast cancer. In the present study, we found that estrogen can activate BRCA2 transcription, which is estrogen receptor (ER) α-dependent. During estrogen treatment, ERα interacted with CREB-binding protein/p300, p68/p72, and MyoD and formed an activating transcriptional complex that could bind to many Sp1 sites on the BRCA2 promoter and activate its transcription by inducing histone acetylations. MyoD is a new component of ERα complex. ERβ or p53 attenuated ERα-mediated transcriptional activation by preventing the recruitment of ERα transcriptional complex and histone acetylations on the BRCA2 promoter. ERβ interacted with ERα and CREB-binding protein/p300 and formed a weak activating transcriptional complex that competed for binding to Sp1 sites with ERα transcriptional complex and slightly attenuated BRCA2 transcription. Different from ERβ, p53 interacted with HDAC1 and CtBP1 and formed an inhibiting transcriptional complex that could compete for binding to Sp1 sites with ERα transcriptional complex and inhibit BRCA2 transcription more significantly
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