ArticleClinical and translational medicine2026
Tumour-macrophage crosstalk initiated by NFIC/METTL3 negative feedback loop via exosomal miR-194-5p promotes NSCLC progression.
Article in Clinical and translational medicine, 2026. 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
backgroundThe interplay between tumour cells and tumour-associated macrophages (TAMs) within the tumour microenvironment is crucial for the progression of non-small cell lung cancer (NSCLC). The underlying mechanisms involving RNA modification and exosomal communication remain incompletely understood.
methodsMultiplex immunofluorescence and flow cytometry were performed to evaluate M2 macrophage polarization. Exosomes were isolated by ultracentrifugation and validated by transmission electron microscopy, nanoparticle tracking analysis, and exosomal marker blots. To investigate the molecular mechanism, methylated RNA immunoprecipitation (MeRIP)-qPCR and dual-luciferase reporter assays were used to validate m
resultsA negative feedback loop between METTL3 and NFIC was demonstrated in NSCLC cells. METTL3 suppressed miR-194-5p expression and its loading into exosomes through m
conclusionsThese findings establish a closed regulatory circuit initiated by an NFIC/METTL3 negative feedback loop. In this circuit, METTL3-mediated m KEY POINTS: NFIC/METTL3 negative feedback loop in NSCLC cells suppresses exosomal miR-194-5p via m6A methylation; reduced miR-194-5p deepresses ZNF106 in macrophages, promoting M2 polarization and IL-6 secretion; Macrophage-derived IL-6 activates JAK2/STAT3 in NSCLC cells to upregulate METTL3, forming a positive feedback loop.
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