Epigenetic and metabolic reprogramming by HDAC inhibition targets NRF2-active tumors [CRISPR Screen]

To identify NRF2-specific dependencies in chromatin regulation, we performed a focused genetic screen mouse LUAD cell lines with or without knock-out of KEAP1. A chromatin-focused CRISPR/Cas9 dropout screen was performed in 2 KP and 2 KPK cell lines and sgRNA enrichment was assessed by deep-sequencing at 0(t0) and 14(t1) population doublings.