Chromatin accessibility changes in experimentally-induced basal to squamous cell carcinoma transition (BST) upon EGFR/MAPK inhibitor treatments [ASZ_ATACseq_inhibitor]

Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST. Alternatively we drive c-FOS to induce BST. Here, we analyze chromatin accessibility profiles upon c-FOS activation Overall design: Methods: ATACseq profiles of ASZ transfected with doxycycline-inducible empty vector (ctrl) and c-FOS containing vector (c-FOS) upon Dox treatment with or without EGFR/MAPK inhibitor treatments, were generated by deep sequencing, in duplicate, using Illumina NovaSeq. The sequence reads that passed quality filters were analyzed using bowtie for alignment and macs2 for peak calling