Genome binding/occupancy profiling by high throughput sequencing
Summary
We describe Nfib as an important regulator of chromatin accessibility in Small cell lung cancer (SCLC).
Overall design
ATAC seq was performed on [1] ex vivo samples from primary tumors and metastases of a mouse model for SCLC (4 samples of each plus technical replicates of 7 samples for a total of 15 samples) [2] cell lines derived from mouse models for SCLC. [3] Nfib loss of function in murine SCLC cell lines (shLuc are controls, sh2 is shRNA that knocks down Nfib) [4] Nfib gain of function in murine SCLC cell lines and human SCLC lines (empty indicates control cells, Nfib indicates cells overexpressing Nfib)