What question did this study set out to answer?

The aim is to explore how metabolic engineering via SLC38A2 can improve glutamine utilization and enhance the antitumor function of CAR-Ms.

April 4, 2026Open Access

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.

Abstract

Metabolic engineering via SLC38A2 restored glutamine fitness and enhanced the antitumor activity of HER2-targeted CAR-Ms, thus providing a promising strategy to boost CAR-M-mediated tumor suppression in solid tumors.

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Cite This Study

Liu et al. (Wed,) studied this question.

synapsesocial.com/papers/69d0adc2659487ece0fa44f3 https://doi.org/https://doi.org/10.20892/j.issn.2095-3941.2025.0775

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