2026/06/14 by Davide Ruggero · 1 voice
Biochemistry, Genetics and Molecular Biology · #PI3K/AKT/mTOR signaling in cancer #Protein Degradation and Inhibitors #Polyamine Metabolism and Applications
paper · doi:10.1172/jci207335
openalex publication_date 2026/06/14 · openalex created_date 2026/06/15 · openalex updated_date 2026/07/27
Cancer proteogenomics has revealed that RNA abundance often poorly predicts protein output, highlighting translation as a central determinant of malignant identity. In this issue of JCI, Mishra et al. showed that pharmacologic inhibition of eIF4E cap binding selectively rewired the prostate cancer translatome, suppressing basal keratin translation while promoting luminal features and renewed sensitivity to hormone therapy. More broadly, the study illustrates how tumors exploit selective translation to maintain lineage plasticity, survival, and therapeutic resistance. Targeting translational dependencies may therefore offer a powerful strategy to dismantle cancer-specific proteomic programs and convert resistant cell states into druggable vulnerabilities.