ArticleFrontiers in immunology2025
SLC43A2-mediated immune cell infiltration: a potential therapeutic target in acute myeloid leukemia.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Tumor cells compete with T cells for methionine by overexpressing SLC43A2 (solute carrier family 43 member 2), leading to T cell exhaustion. However, the correlation between SLC43A2 and immune infiltration or malignant features in acute myeloid leukemia (AML) has rarely been explored. Methods: We obtained gene expression data and clinical information from 173 AML patients in The Cancer Genome Atlas (TCGA) database. Statistical analyses were performed using R (v4.0.5). Differential expression, immune infiltration, functional enrichment, and survival analyses were conducted using online databases, including GEPIA, GSCA Lite, Kaplan-Meier Plotter, KEGG, and TIMER2. Results: SLC43A2 was highly expressed in AML and associated with poorer survival. Enrichment analysis revealed that SLC43A2 is involved in lymphocyte activation, leukocyte adhesion, and immune response regulatory signaling pathways. Immune infiltration results showed that SLC43A2 positively correlated with immune exhaustion markers (all p < 0.05) and negatively correlated with CD8+ T, NK, and B cell infiltration (all p < 0.05). We constructed an SPI1-hsa-miR-31-5p-SLC43A2 transcriptional network to support the role of SLC43A2. Conclusion: The SLC43A2 gene may serve as a diagnostic, prognostic, and potential immune-related biomarker for AML patients. Blocking SLC43A2-associated signaling pathways could provide novel insights into immunotherapy for AML.
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