Bulk-ATAC sequencing in RUNX-altered murine lung adenocarcinoma cell lines
Here, we using CRISPR activation and knockout studies to assess the implication of dysregulation of RUNX transcription factors on chromatin accessibility using bulk ATAC-sequencing. Tumor cell lines were derived from primary Kras G12D; p53 mutant mice (KP model) after initiation of tumors with SPC-Cre, resulting in lung adenocarcinoma. Cell lines were then expanded and profiled using bulk ATAC-sequencing. Overall design: Primary tumor derived cell lines were modified using CRISPR knockout and activation. Bulk ATAC-sequencing was completed on these cell lines.