Mitochondrial Translation Inhibition Uncovers a Critical Metabolic-Epigenetic Interface in Renal Cell Carcinoma.

ABSTRACT: Background/Objectives: Renal cell carcinoma (RCC) exhibits distinctive metabolic vulnerabilities that may be therapeutically targeted. This study investigates how tigecycline, an FDA-approved antibiotic that inhibits mitochondrial translation, affects RCC cells and explores potential combinatorial approaches to enhance its efficacy. Methods: We employed comprehensive metabolomic profiling, subcellular proteomics, and functional assays to characterize the effects of tigecycline on RCC cell lines, patient-derived organoids, and xenograft models. The synergistic potential of tigecycline with the histone deacetylase inhibitor entinostat was evaluated using combination index analysis. Results: Tigecycline selectively inhibited mitochondrial translation in RCC cells, reducin

SUBMITTER: Eckenstein K 

PROVIDER: S-EPMC12195425 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature