Although the MAPK pathway drives proliferation in RAS- or RAF-mutant cancers, small-molecule RAF and MEK inhibitors have had limited success in treating RAS- or RAF-mutant cancers. Using genome-scale CRISPR-Cas9 resistance screens, Wang et al. identify the AXN1L-CIC-ETS transcription factor axis as a mediator of resistance to MAPK pathway inhibition.
The authors analyzed the genome-wide effects of TALE- and CRISPR-based transcriptional activators in human cells. Their results show that these transcription factors are highly specific in both DNA-binding and gene regulation, and are able to open targeted regions of closed chromatin independent of gene activation. Collectively, these results underscore the potential for these technologies to make precise changes to gene expression for gene and cell therapies or fundamental studies of gene function.
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Although the MAPK pathway drives proliferation in RAS- or RAF-mutant cancers, small-molecule
RAF and MEK inhibitors have had limited success in treating RAS- or RAF-mutant cancers.
Using genome-scale CRISPR-Cas9 resistance screens, Wang et al. identify the AXN1L-CIC-ETS
transcription factor axis as a mediator of resistance to MAPK pathway inhibition.