Resumen
Aerobic glycolysis is a key driving force of tumorigenesis and chemoresistance. Girdin plays a vital role in cancer cells; however, the role of Girdin in aerobic glycolysis is still unclear. In this study, we first found that knockout of Girdin markedly inhibited lung adenocarcinoma (LUAD) progression in an autochthonous LUAD mouse model. In addition, we found that Girdin interacted with pyruvate kinase M2 (PKM2) and impaired PKM2 activity, which promoted the Warburg effect and chemoresistance. Our results suggest that Girdin is a potential therapeutic target to overcome the resistance of LUAD cells to chemotherapeutic agents.