Metabolic engineering of SLC38A2 reprograms glutamine utilization and enhances CAR-macrophage antitumor function in solid tumors

Key Points

• The aim is to explore how metabolic engineering via SLC38A2 can improve glutamine utilization and enhance the antitumor function of CAR-Ms.
• Utilized metabolic engineering to modify SLC38A2 expression.
• Assessed glutamine fitness in targeted CAR-Macrophages.
• Evaluated antitumor activity against HER2-targeted solid tumors.
• Restoration of glutamine utilization was achieved.
• Enhanced antitumor activity of CAR-Macrophages was observed.
• Demonstrated potential for improved tumor suppression in solid tumors.