Fig. 3: PRMT1 physically associates with the FOXA1 and HNF4G interactome.

a, Volcano plot represents FOXA1-RIME candidates discovered in HPAF-II cells. The average of identified peptides in three biological replicates was calculated and proteins absent in IgG control samples were filtered for <3 unique peptides, P values of 0.003. Proteins of interest are highlighted. b, Signal intensity plots generated from PRMT1 ChIP–seq in control and HNF4G-KO binding regions. c, Intensities of PRMT1 binding coverage measured at open sites (H3K27Ac) in proximity to HNF4G-regulated genes found in control, HNF4G-KO, HNF4G-KO + rescue conditions. d, ChIP–seq tag density heatmap of FOXA1, HNF4G and PRMT1 co-occupancy at PRMT1 binding sites from a representative patient tumor sample. Venn diagram is an overlap of binding sites of these factors from one representative patient. Panel d was created with BioRender.com. e, Distance correlation heatmap of ChIP–seq locations illustrates cobinding similarity of PRMT1, FOXA1 and HNF4G from three independent Whipple surgical samples. f,g, Control and HNF4G-KO cells were orthotopically implanted into the pancreas of mice. Mice with palpable tumors were then randomized into four groups and treated with GSK3368715 (oral administration of 75 mg kg⁻¹ five doses per week) for 4 weeks, with n = 9 mice for control vehicle and HNF4G-KO vehicle arms and for control + GSK3368715 and HNF4G-KO + GSK3368715 arms n = 12. *P = 0.0339, ***P < 0.0001 and ***P = 0.0002 were calculated with a Welch test with multiplicity corrections (f). **P = 0.003, ***P = 0.0001 and ***P < 0.0001 of random intercept piecewise model parameters were defined by means of Wald t tests (g). The lighter lines indicate mouse-specific longitudinal tumor volume measures, color-coded by specific groups.