TL;DR
In vivo experiments demonstrated that exosomes from EHF-silenced M2 macrophages inhibited tumor growth and downregulated proliferation markers, and highlighted the EHF/FGFR1 axis as a novel molecular link between macrophages and NSCLC cells.
It is demonstrated that lactate derived from CAFs promotes the expression of stemness genes by mediating H3K18 lactylation in the promoters of these genes in NSCLC cells, thereby accelerating the malignant phenotype formation of NSCLC cells.
This study uncovers a divergent metabolic program mediated by HMGB1 and demonstrates its role in lysosomal metabolic plasticity in tumors and in macrophages.
Current insights into exosome-driven macrophage polarization in HCC are summarized, providing a potential immunotherapeutic strategy for restoring antitumor immunity and improving HCC patient prognosis.
A novel mechanism by which FOXP1 transcriptionally upregulates NUSAP1 expression results in glycolytic metabolic reprogramming that induces TAM M2 polarization and promotes HCC progression, identifying a potential therapeutic avenue for reversing the immunosuppressive microenvironment in HCC.
Thrombospondin 1 regulates pathological interorgan communication between GC cells and the peritoneal niche by targeting TAMs through metabolic reprogramming, thereby providing a potential therapeutic target for GC with PM and insights into interorgan metastasis mechanisms.
WNK4 acts as an immune-relevant suppressor in endometrial cancer, partly by limiting M2-like polarization and weakening macrophage-driven tumor support, partly by limiting M2-like polarization and weakening macrophage-driven tumor support.
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