~50% of colorectal cancers have an activating mutation in KRAS (encoding the KRAS proto-oncogene) and remain difficult to target in the clinic. We have recently shown that activation of KRAS protein alters the regulation of mRNA translation, increasing total protein synthesis, and maintaining elevated c-MYC (MYC proto-oncogene) expression. Targeting these pathways downstream of KRAS reveals a striking dependency that has potential for clinical translation.
Keywords: KRAS mutation; MYC; Protein synthesis; colorectal cancer; eIF4E.
© 2021 The Author(s). Published with license by Taylor & Francis Group, LLC.