Fig. 7: The model of RAC1 on ER transcriptional activity.

A In the absence of estrogen, there is little ER-RAC1 complex on chromatin. B Estrogen-bound ER dimer brings its coactivator SRC-3, RAC1 as well as RNA pol II to ER binding sites to activate gene transcription. C In the presence of RAC1 inhibitor only, ER-RAC1 complex is stabilized on chromatin; RNA pol II is accumulated at ER binding sites and promoters of ER target genes. D In the presence of both estrogen and RAC1 inhibitor, ER complex including SRC-3 and RAC1 is stabilized on chromatin; RNA pol II, which fails to activate gene transcription, is accumulated at ER binding sites and promoters of ER target genes. ER transcriptional activity is blocked by RAC1 inhibitor, which is distinct to anti-estrogens and prevents the interaction between ER and its coactivator SRC-3. RAC1 inhibition provides an alternative way to attenuate ER transcriptional activity. The figure was created with BioRender.com.