BRCA2 is closely related to the pathogenesis of breast cancer. In the present report, we find that estrogen can activate BRCA2 transcription, which is ERa-dependent. During estrogen treatment, ERa interacts with CBP/p300, p68/p72, MyoD and forms an activating transcriptional complex which can bind to many Sp1 sites on the BRCA2 promoter and activate its transcription by inducing histone acetylations; MyoD is a new component of ERa complex; ERß or P53 attenuates ERa-mediated transcriptional activation by preventing the recruitment of ERa transcriptional complex and histone acetylations on the BRCA2 promoter; ERß interacts with ERa, CBP/p300 and forms a weak activating transcriptional complex which competes for binding to Sp1 sites with ERa transcriptional complex and slightly attenuates BRCA2 transcription; Different from ERß, p53 interacts with HDAC1 and CtBP1 and forms an inhibiting transcriptional complex which can compete for binding to Sp1 sites with ERa transcriptional complex and inhibit BRCA2 transcription more significantly.