ArticleJournal of clinical biochemistry and nutrition2026
METTL3-mediated m6A modification of CXCR4 drives M2 macrophage polarization and suppresses anti-tumor immunity in esophageal cancer.
Article in Journal of clinical biochemistry and nutrition, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- METTL3 in esophageal cancer: Current insights into molecular mechanisms, subtype heterogeneity and targeted therapy prospects (Review).International journal of oncology · 2026Review
- Enhancing targeted strategies for cancer immunotherapy by elucidating mRNA processing mechanisms.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dense tumor-associated macrophage infiltration correlates with poor prognosis in esophageal cancer (EC), yet the underlying molecular mechanisms remain undefined. An EC cell-macrophage co-culture system was established. M2 polarization was evaluated by flow cytometry and ELISA. qPCR and Western blot were employed to detect mRNA and protein levels. MeRIP-PCR assessed CXCR4 m6A methylation. Colony formation, wound-healing, and apoptosis assays measured EC cell proliferation, migration, and apoptosis. Compared with macrophages co-cultured with normal esophageal epithelial cells, those co-cultured with EC cells exhibited increased IL-10 and TGF-β secretion, accompanied by up-regulation of CD206, CD163, CXCR4, and METTL3. METTL3 up-regulated CXCR4 by mediating CXCR4 m6A methylation. METTL3-overexpressing macrophages elevated CD206/CD163 levels and IL-10/TGF-β secretion, whereas CXCR4 knockdown reversed these effects. Moreover, METTL3-high macrophages promoted EC cell proliferation and migration, up-regulated PD-L1, and inhibited apoptosis. METTL3 is up-regulated in EC-associated macrophages, promotes M2 polarization via m6A modification of CXCR4, and thereby accelerates EC malignant progression.
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Registered trials
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