Author:

Keywords:

Science & Technology, Life Sciences & Biomedicine, Biochemistry & Molecular Biology, AMINO-ACID-METABOLISM, TUMOR MICROENVIRONMENT, GLUTAMINE UPTAKE, ACTIVATION, EXPRESSION, SERINE, PD-1, PROLIFERATION, CHECKPOINT, EXHAUSTION, antitumorigenic T cells, immunometabolism, protumorigenic T cells, tumor microenvironment, Humans, CD8-Positive T-Lymphocytes, Tumor Microenvironment, Neoplasms, G065122N#56765316, C14/22/115#57006280, 03 Chemical Sciences, 06 Biological Sciences, 11 Medical and Health Sciences, Developmental Biology, 3101 Biochemistry and cell biology, 3205 Medical biochemistry and metabolomics, 3404 Medicinal and biomolecular chemistry

Abstract:

The metabolic cross-talk between cancer cells and T cells dictates cancer formation and progression. These cells possess metabolic plasticity. Thus, they adapt their metabolic profile to meet their phenotypic requirements. However, the nutrient microenvironment of a tumor is a very hostile niche in which these cells are forced to compete for the available nutrients. The hyperactive metabolism of tumor cells often outcompetes the antitumorigenic CD8+ T cells while promoting the protumorigenic exhausted CD8+ T cells and T regulatory (Treg) cells. Thus, cancer cells elude the immune response and spread in an uncontrolled manner. Identifying the metabolic pathways necessary to shift the balance from a protumorigenic to an antitumorigenic immune phenotype is essential to potentiate antitumor immunity.