Deletion of ENO1 sensitizes pancreatic cancer cells to gemcitabine via MYC/RRM1-mediated glycolysis.

ABSTRACT: Glycolysis is a critical metabolic pathway in cancer cells, fulfilling their energy requirements, supporting biosynthesis, maintaining redox balance, and enabling survival in hostile environments. Alpha-enolase (ENO1) has been identified as a key promoter of tumor progression through its involvement in glycolysis. This study aims to elucidate the relationship between ENO1, glycolysis, and gemcitabine sensitivity in pancreatic cancer (PC). The expression levels of ENO1 in PC were analyzed using the GEPIA2 database, Kaplan-Meier survival plots, and immunohistochemistry (IHC). To assess the impact of ENO1 on gemcitabine sensitivity, we manipulated ENO1 expression in PC cell lines through overexpression and silencing techniques. Subsequent analyses included flow cytometry assays, glucose uptak

SUBMITTER: Lu Y 

PROVIDER: S-EPMC11929750 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature