Fig. 8: Tryptase affects chromatin accessibility in breast cancer cells.

ATAC-seq analysis of Hs578T breast cancer cells cultured for 6 or 24 h under normal conditions (Control 1-3) or with 50 nM tryptase (Tryptase 1-3). A Distribution of genomic features assigned to peaks as exon, intergenic, intron, promoter-TSS (transcription starting site), Transcription termination site (TTS) and unassigned. B Mapped reads per counts for each chromosome (y-axis, number of mapped reads). C Heatmap of the sample-to-sample distances amongst replicates from control and tryptase-treated samples. D Number of peaks with decreased (blue) or increased (red) chromatin accessibility. A total of 2,619 genomic intervals were mapped in the analysis. E Chromatin accessibility results for control (blue) and tryptase-treated (purple) samples mapped to genes of interest (CCN1, CCN2, ARRDC3, Mir591). A histone mark reference track generated by a compilation of several ChIP-seq studies obtained from ChIP Atlas (www.chip-atlas.org) is displayed in yellow. Peaks are shown as overlayed replicates for each group (control and tryptase). F Western blot analysis of H3K27ac, with densitometry quantification normalized to GAPDH and expressed as a percentage of the control. Statistical significance was determined by unpaired t-test; *p ≤ 0.05. G Immunofluorescence staining for H3K27ac in control and tryptase-treated Hs578T cells after 48 h. Nuclei were visualized with Hoechst 33342 staining. Scale bar: 20 μm.