Scientists have found that deficiency of two key glycolytic enzymes, Glut1 (glucose transporter 1) and Gpi1 (glucose-6-phosphate isomerase 1), enhanced tumor cell killing by cytotoxic T cells. Genetic and pharmacologic inactivation of Glut1 sensitizes tumors to anti-tumor immunity and synergizes with anti-PD-1 therapy through the TNF-α pathway. |
Tumor aerobic glycolysis confers immune evasion through modulating sensitivity to T cell-mediated bystander killing via TNF-α Point of Interest - Depletion of Glut1 sensitizes tumor cells to cell death induced by TNF-α through the augmentation of reactive oxygen species (ROS). - Glut1 and Glut3 exhibit differential expression in tumor cells compared to immune cells. - Inhibiting Glut1 enhances the anti-tumor immune response in murine models. |
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Metabolic shift to glycolysis in senescenct cells |
<Evaluation by Lactate production and ATP levels>
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