ArticleCancer innovation2022
Prognostic value of lactate transporter SLC16A1 and SLC16A3 as oncoimmunological biomarkers associating tumor metabolism and immune evasion in glioma.
Article in Cancer innovation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- The formation and function of tertiary lymphoid structures.Biomarker research · 2026Review
- Targeting Glycolytic Metabolism in Cancer Therapy: Current Approaches and Future Perspectives.Cells · 2026Review
- Metabolic reprogramming and immune evasion interaction in the tumor microenvironment promote tumor progression.Frontiers in oncology · 2026Review
- Molecular mechanisms and clinical significance of the glioma metabolic-immune axis: a comprehensive review.Frontiers in immunology · 2026Review
- SLC16A3 in lung adenocarcinoma regulates glycolysis and lactate release to facilitate M2 polarization of tumor-associated macrophages : Short Title: SLC16A3 reinforces macrophage M2 polarization through glycolysis.Cancer immunology, immunotherapy : CII · 2025Article
- Integrated single-cell and bulk RNA-sequencing data reveal prognosis and therapeutic response in low-grade glioma based on hypoxia-lactylation related genes.Discover oncology · 2025Article
- Advances in Cellular Immune Theranostic Approaches for Glioblastoma: Current Trends and Future Directions.Cancer innovation · 2025Review
- SLC16A3 (MCT4) expression in tumor immunity and Metabolism: Insights from pan-cancer analysis.Biochemistry and biophysics reports · 2025Article
- Precision Nanotherapy for Spinal Cord Injury: Modulating SLC16A3 With Methylprednisolone-Loaded Nanoparticles.Neurospine · 2025Article
- Angiogenesis and targeted therapy in the tumour microenvironment: From basic to clinical practice.Clinical and translational medicine · 2025Review
- SLC16A3 drives lung adenocarcinoma progression and gefitinib resistance through coordinated regulation of ferroptosis and lactate metabolism.Frontiers in immunology · 2025Article
- Identification of key ferroptosis-related genes and therapeutic target in nasopharyngeal carcinoma.Frontiers in genetics · 2025Article
- Defining solute carrier transporter signatures of murine immune cell subsets.Frontiers in immunology · 2023Article
- Prognostic value of lactate transporter SLC16A1 and SLC16A3 as oncoimmunological biomarkers associating tumor metabolism and immune evasion in glioma.Cancer innovation · 2022Article
- Targeting immune microenvironment-mediated mesenchymal transition in glioblastoma: Molecular mechanisms and translational strategies.Neuro-oncology advancesReview
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hypoxic microenvironment is immunosuppressive and protumorigenic, and elevated lactate is an intermediary in the modulation of immune responses. However, as critical lactate transporters, the role of SLC16A1 and SLC16A3 in immune infiltration and evasion of glioma is not fully elucidated. Methods: Gene expression in low- and high-grade glioma (LGG and GBM) was evaluated with TCGA database. The TISIDB, TIMER and CIBERSORT databases were utilized for the analysis of the correlation between SLC16A1 or SLC16A3 and immunocyte infiltration as well as immune checkpoints. Results: Compared with normal tissues, a significant increase of both SLC16A1 and SLC16A3 was found in LGG and GBM, and closely related to the poor prognosis only in LGG. Cancer SEA indicated that SLC16A1 was involved in hypoxia while SLC16A3 contributed to metastasis and inflammation in glioma. The SLC16A3 expression was significantly correlated with neutrophil activation by GO analysis. TISCH showed the distribution of SLC16A1 on glioma cells and SLC16A3 on immune cells, which was correlated to tumor-associated macrophages and neutrophils that are immunosuppressive. SLC16A1 and SLC16A3 were identified to tightly interacted with diverse immune checkpoints (especially PD1, PD-L1, PD-L2, Tim-3) and immunosuppressive factors (TGF-β and IL-10) in glioma. Furthermore, SLC16A3 had a positive correlation to activation markers of tumor-associated neutrophils and chemokines such as CCL2, CCL22, CXCR2, CXCR4 in LGG and CCL7, CCL20 CXCL8 in GBM, which could enhance infiltration of immunosuppressive cells to the tumor microenvironment. Conclusion: In general, our results suggest that SLC16A1 and SLC16A3 act as a bridge between tumor metabolism and immunity by promoting immunosuppressive cell infiltration, which contributes to immune evasion and a worse prognosis in glioma. Targeting SLC16A1 and SLC16A3 may provide novel therapeutic strategy for immunotherapy in glioma.
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