GSE96780
Genome-wide maps of histone H3K27 acetylation in A549 and MSR-A549 cells.
To establish effective multitargeted KRAS pathway therapy, we analyzed mediators of acquired resistance to chronic momelotinib and MEK inhibitor exposure in A549 cells. Since inhibitor resistance was completely reversible after drug withdrawal for several passages, suggesting epigenetic reprogramming, we examined genome-wide H3K27 histone acetylation in parental A549 and momelotinib and selumetinib resistant (MSR)-A549 cells. Overall design: Examination of histone H3K27 acetylation in A549 and MSR-A549 cells.