ArticleFrontiers in cell and developmental biology2025
Lactate modulates the function of myeloid-derived suppressor cells via Ten-Eleven-Translocation-2-mediated demethylation of glucocorticoid-inducible kinase 1 in lung cancer model.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Research progress on lactate metabolism in lung cancer: Tumorigenesis, drug resistance and clinical translation (Review).Oncology reports · 2026Review
- Stem cells as an essential mediator of the exercise-tumorigenesis link.Nature reviews. Cancer · 2026Review
- Lactate signaling and immune suppression in tumors: mechanisms and therapeutic implications.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Lactate, a Spearhead of Cancer Aggressiveness: Metabolic Reprogramming, Immune Suppression, and Metastatic Progression.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2026Review
- The lactylation axis: bridging metabolic reprogramming and immunosuppression in the tumor microenvironment.Frontiers in immunology · 2026Review
- Metabolic licensing and restriction of innate immunity in the tumor microenvironment.Frontiers in immunology · 2026Review
- Lactate and lactylation in cancer: drivers of immune suppression and microenvironmental reprogramming.Experimental hematology & oncology · 2025Review
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Abstract
Background: Lactate has been shown to play an important immunosuppressive role in the tumor microenvironment (TME) and promote tumor progression through a variety of different mechanisms of action. Myeloid-derived suppressor cells (MDSCs) are important cells that play an immunosuppressive role in the TME. However, the underlying mechanism by which lactate regulates MDSCs remains unclear. This study aims to explore the molecular mechanism by which lactate regulates the immunosuppressive function of MDSCs in the TME, providing new ideas and targets for anti-tumor immunotherapy targeting MDSCs. Methods: This study used the Lewis lung carcinoma cell line to establish a subcutaneous lung cancer model; MDSCs were isolated from the spleens of these mice for subsequent experiments. Protein expression was analyzed by Western blot, mRNA expression by qRT-PCR, protein-DNA interactions by ChIP-qPCR, and DNA methylation by MSP-qPCR and BSP. Exploring the regulatory mechanism of CD38 on the immunosuppressive function of MDSCs by knockdown and overexpression techniques. Results: We found that compared with spleen-derived MDSCs (SP-MDSCs) of subcutaneous lung cancer model, tumor-derived MDSCs (T-MDSCs) had stronger immunosuppressive function. Lactate could promote the immunosuppressive function of MDSCs, significantly upregulate the expression of serum and glucocorticoid-inducible kinase 1 (SGK1) in MDSCs. Further studies demonstrated that lactate could downregulate the DNA methylation level of SGK1 by regulating the Ten-Eleven-Translocation-2 (TET2) and TET2 was closely related to the immunosuppressive function of MDSCs and the progression of tumors. Conclusion: Lactate can upregulate the expression of SGK1 through demethylation mediated by TET2, enhancing the immunosuppressive function of MDSCs to promote tumor progression. It provides the effective therapeutic targets for anti-tumor therapy.
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