GSE161009
Chromatin accessibility changes in experimentally-induced basal to squamous cell carcinoma transition (BST)
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. In these various experimentally-induced model of BST, we analyze chromatin accessibility profiles upon Ras/MAPK activation and/or TGFb signaling abrogation. We also analyze chromatin accessibility profiles upon c-FOS activation. Overall design: RasV12-expressing and/or TGFbR1-kd ASZcells were processed for ATAC-seq. Two biological replicates were sequenced  per treatment group. ATACseq profiles of ASZ transfected with doxycycline-inducible empty vector (ctrl) or c-FOS containing vector (c-FOS) upon Dox treatment, were generated by deep sequencing, in duplicate, using Illumina NextSeq. The sequence reads that passed quality filters were analyzed using bowtie for alignment and macs2 for peak calling.