ArticleFrontiers in immunology2022
Epigenetic therapy reprograms M2-type tumor-associated macrophages into an M1-like phenotype by upregulating miR-7083-5p.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 27 citations in OpenAlex.
- Beyond the genetic code: orchestrating epigenetic and immune landscapes with multivalent mRNA-exosome vaccines.Precision clinical medicine · 2026Review
- Targeting the cytokine-epigenetic axis: a new paradigm and prospects for disease treatment.European cytokine network · 2026Review
- ORY1001 enhances anti-tumor immunity via CXCL10-mediated macrophage modulation in EBV-positive DLBCL.Cell communication and signaling : CCS · 2026Article
- Review
- Macrophages in Colorectal Cancer: from Normal Mucosa to Distant Metastasis: Beyond the M1/M2 Paradigm.Journal of Cancer · 2026Review
- Targeting the Dynamics Between TAMs and CAR-T Cells in Solid Tumor Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Epigenetics in Ovarian Cancer: A Review of Current Knowledge and Future Perspectives.Biomedicines · 2025Review
- Combination immunotherapy in hepatocellular carcinoma: synergies among immune checkpoints, TKIs, and chemotherapy.Journal of hematology & oncology · 2025Review
- Review
- Review
- The Role of Lactate and Lactylation in the Dysregulation of Immune Responses in Psoriasis.Clinical reviews in allergy & immunology · 2025Review
- The epigenetic hallmarks of immune cells in cancer.Molecular cancer · 2025Review
- The role of macrophages in liver metastasis: mechanisms and therapeutic prospects.Frontiers in immunology · 2025Review
- An Epic Advancement in Targeting Macrophages for Cancer Therapy Approach.Current drug delivery · 2025Review
- Emerging macrophage-based therapies for cancer: a review of preclinical and clinical advances.Frontiers in immunology · 2025Review
- Review
- Review
- Deciphering the performance of macrophages in tumour microenvironment: a call for precision immunotherapy.Journal of hematology & oncology · 2024Review
- Apoptosis, a Metabolic "Head-to-Head" between Tumor and T Cells: Implications for Immunotherapy.Cells · 2024Review
- Plasma Cell-Free Tumor Methylome as a Biomarker in Solid Tumors: Biology and Applications.Current oncology (Toronto, Ont.) · 2024Review
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Reprogramming M2-type, pro-tumoral tumor-associated macrophages (TAMs) into M1-type, anti-tumoral macrophages is a key strategy in cancer therapy. In this study, we exploited epigenetic therapy using the DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-aza-dC) and the histone deacetylation inhibitor trichostatin A (TSA), to reprogram M2-type macrophages into an M1-like phenotype. Treatment of M2-type macrophages with the combination of 5-aza-dC and TSA decreased the levels of M2 macrophage cytokines while increasing those of M1 macrophage cytokines, as compared to the use of either therapy alone. Conditioned medium of M2 macrophages treated with the combination of 5-aza-dC and TSA sensitized the tumor cells to paclitaxel. Moreover, treatment with the combination inhibited tumor growth and improved anti-tumor immunity in the tumor microenvironment. Depletion of macrophages reduced the anti-tumor growth activity of the combination therapy. Profiling of miRNAs revealed that the expression of miR-7083-5p was remarkably upregulated in M2 macrophages, following treatment with 5-aza-dC and TSA. Transfection of miR-7083-5p reprogrammed the M2-type macrophages towards an M1-like phenotype, and adoptive transfer of M2 macrophages pre-treated with miR-7083-5p into mice inhibited tumor growth. miR-7083-5p inhibited the expression of colony-stimulating factor 2 receptor alpha and CD43 as candidate targets. These results show that epigenetic therapy upon treatment with the combination of 5-aza-dC and TSA skews M2-type TAMs towards the M1-like phenotype by upregulating miR-7083-5p, which contributes to the inhibition of tumor growth.
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