Fig 2: SWI/SNF mediates activation of PGR expression following E2 stimulation. (A) Rank visualization of top estrogen-regulated genes in 12Z-ESR1 cells. Red indicates upregulated genes, blue indicates downregulated genes. (B) Western blot analysis in 12Z-ESR1 cells following treatment with E2, siARID1A, or both E2 and siARID1A for ARID1A, PGR, and ESR1. PGR isoforms are indicated by arrowheads. β-Actin was used as a loading control. Blot is representative of 4 independent experiments. (C) Densitometry analysis of protein expression of ARID1A, PGR, and ESR1 following western blot as in panel B for control (silver), E2 (yellow), siARID1A (green) and siARID1A + E2 (pink). Densitometry values were normalized to β-Actin. Means ± SDs, n = 3–4. The paired t-test was used for analysis. (D) Western blot analysis in 12Z-ESR1 cells following treatment with E2, siBRG1, siARID1B, siBRG1+E2, or siARID1B+E2 for ARID1B, BRG1, PGR, and ESR1. PGR isoforms are indicated by arrowheads. β-Actin was used as a loading control. Blot is representative of 4 independent experiments. (E) Densitometry analysis of protein expression of ARID1B, BRG1, PGR, and ESR1 following western blot as in panel D for control (silver), E2 (yellow), siARID1B (charcoal), siARID1B + E2 (red), siBRG1 (brown) and siBRG1 + E2 (purple). Densitometry values were normalized to β-Actin. Means ± SDs, n = 4–5. The statistic is paired t-test. * p < 0.05; n.s. is non-significant.

Fig 3: Identification of specific mutations of SMARCA4 in CRC patients.a Oncoprint plot showing the genomic profiles of SMARCA4, SMARCA2, SMARCB1, SMARCC1, SMARCC2, SMARCE1, ARID1A, ARID1B, and other CRC relevant genes, data compiled from the cBioPortal based on original data from TCGA CRC project. b Detection of the SMARCA4 gene showing the c. 3721C>T (p. Arg1157Trp) mutation in tumor samples of CRC patients using DNA sequencing.

Fig 4: Arid1b is indispensable for OD differentiation but is not involved in Hh signaling regulation(A and B) Immunofluorescence of Arid1b of first mandibular molars of control and Gli1-CreER;Arid1afl/fl mice at PN7.5.(C) Western blot of Arid1b in the apical region of the first mandibular molars from control and Gli1-CreER;Arid1afl/fl mice at PN7.5.(D) UCSC Genome Browser screenshot of Arid1b at the Gli1 locus and ChIP assay with Arid1b antibody (or IgG), followed by qPCR. n = 3, *p < 0.05.(E) Western blot of Gli1 and Ccnd1 in DPCs with control siRNA or four different Arid1b siRNA sets.(F) Western blot of Gli1 and Ccnd1 in DPCs with control siRNA, Arid1a siRNA, or both Arid1a and Arid1b siRNA.(G) Western blot of Dspp and Dmp1 in DPCs with control siRNA or four different Arid1b siRNA after odontogenic induction.(H) Alizarin red S staining of DPCs with control siRNA or four different Arid1b siRNA after odontogenic induction. Schematic indicates induction protocol. Scale bars: 100 µm.

Fig 5: Arid1a ablation silences the enhancer of the A20 gene to stimulate NF-?B signaling.a Relative expressions of SWI/SNF components in epithelium from 12-week-old PtenPC-/- and PtenPC-/-; Arid1aPC-/- prostates (n = 3). b Heatmap of H3K27ac ChIP-seq in the differentially accessible sites obtained by ATAC-seq on Arid1a loss in Myc-CaP cells (± 2 kb regions centered at the peak summit). PC, peak center. c Heatmap of the ChIP-seq profiles of BRG1 peaks in control and Arid1a KO Myc-CaP cells shown in a horizontal window of ±2 kb from the peak center. d Profile and bar plot of BRG1 binding, H3K27ac modification and ATAC-seq intensities across BRG1 down peaks after Arid1a ablation. e ChIP-seq profiles for BRG1, H3K4me3, H3K4me1 and H3K27ac at the sites reducing BRG1 binding after Arid1a loss. f Venn diagram of the genes showing reduced BRG1 binding, accessibility and expression in Arid1a KO Myc-CaP cells compared to WT cells. g ChIP-seq tracks of BRG1, H3K27ac, H3K4me1, H3K4me3 and ATAC-seq signals in A20 gene loci as indicated. h ChIP-qPCR assays of BRG1, BAF155, ARID1A and ARID1B binding in the A20 enhancer (n = 3), ns, no significance. i IB analysis of the indicated protein in WT and Arid1a KO Myc-CaP cells with or without A20 enhancer activation (CRISPRa/dCas9-based induction) and/or TNFa stimulation. j IB analysis in WT and ARID1A overexpressing Myc-CaP cells with or without A20 enhancer suppression (CRISPRi/dCas9-based suppression) and/or TNFa stimulation. k Tumor volume of the mice inoculated with Myc-CaP expressing sgArid1a and control vector with or without A20 enhancer activation (WT/Arid1a KO + Ctrl-sgRNA and WT + Enhancer-sgRNA, n = 7 for each group; Arid1a KO + Enhancer-sgRNA, n = 5). a, d, h, k Data represent the mean ± SEM. Statistical significance was determined by two-tailed unpaired t-test (a, d, h) and two-way ANOVA followed by multiple comparisons (k). i, j Experiments were repeated three times independently with similar results; data from one representative experiment are shown. ns, no significance. Source data are provided as a Source Data file.