Elevated co-expression of TIMM17A and NMT1 is associated with poor survival in non-small cell lung cancer.

ABSTRACT: Lung carcinoma cells harboring mutations in STK11 and/or KEAP1 in a KRAS mutant background have intrinsic therapeutic resistance. We found that these cells are sensitive to preclinical stage pharmacological inhibitors of N-myristoyltransferases, which reduce tumor growth in xenograft mouse models. Unexpectedly, the sensitivity to NMT inhibitors correlates with cell's dependency on the inner mitochondrial protein Translocase of Inner Mitochondrial Membrane 17 A (Protein: TIM17A, Gene: TIMM17A). Leveraging data from The Cancer Genome Atlas (TCGA), we set to further explore the significance of N-myristoyltransferase-1 (NMT1) and TIMM17A expression individually and together in cox-regression models to test their association to clinical endpoints in lung carcinoma. Our results showed that lung

SUBMITTER: Chan AA 

PROVIDER: S-EPMC12518850 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature