Highlights • The glutamine utilization of KRAS-mutant NSCLC is higher than that of KRAS wild-type.• Targeted GLS1 and MEK inhibition enhance antitumor activity in vitro and in vivo.• The therapeutic… Click to show full abstract
Highlights • The glutamine utilization of KRAS-mutant NSCLC is higher than that of KRAS wild-type.• Targeted GLS1 and MEK inhibition enhance antitumor activity in vitro and in vivo.• The therapeutic response can be well identified by 18F-FDG PET imaging.• Dual inhibition of GLS1 and MEK induce redox and energetic stress.• Dual inhibition of GLS1 and MEK suppress the phosphorylation of AKT.
               
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