Extended Data Fig. 7|. K270R mutation of FOXA1 enhances the chromatin binding of FOXA1 and subsequently stabilizes AR recruitment.

a, LNCaP-tetFOXA1^WT cells treated with GSK2879552 (50μM) were fractionated into the soluble nuclear fraction and the insoluble chromatin-bound fraction, followed by immunoblotting for V5 and histone 3 (H3). b, CWR22RV1-tetFOXA1^WT or CWR22RV1-tetFOXA1^K270R cells were fractionated into the soluble nuclear fraction and the insoluble chromatin-bound fraction, followed by immunoblotting for V5 and H3. c, LNCaP-tetFOXA1^WT or LNCaP-tetFOXA1^K270R cells were treated with/out doxycycline for 48h, and DHT or vehicle for 4h. ChIP-qPCR for AR binding at AR-regulated enhancers was shown. d, ChIP-qPCR for AR binding in LNCaP-tetFOXA1^WT or LNCaP-tetFOXA1^K270R cells treated with DHT (10nM) versus DHT plus enzalutamide (10μM). e, qRT-PCR for androgen-induced gene expression in response to enzalutamide treatment in CWR22RV1-tetFOXA1^WT or CWR22RV1-tetFOXA1^K270R cells (in the presence of 10nM DHT). Note: Experiments described in this figure were all done under hormone-depleted conditions.