TL;DR
Findings indicate that exosomal ETS2 promotes CRC progression and M2 macrophage polarization via PRPF4, highlighting the ETS2/PRPF4 axis as a potential therapeutic target.
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 suggested that GNAS-AS1 may contribute to the maintenance of M2-like characteristics in TAMs and facilitate CC progression, potentially through a mechanism involving miR-518c-5p sequestering, FBXO38 upregulation, and subsequent modulation of MAPK signaling.
Exosomal METTL16 from AML-MSCs plays a crucial role in promoting leukemic cell survival and M2 polarization, and targeting this axis may provide a potential theoretical foundation to reverse M2 macrophage polarization and inhibit AML progression.
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.
Serving as a highly prevalent malignant tumor, lung adenocarcinoma (LUAD) is frequently associated with the establishment of an immunosuppressive tumor microenvironment during its initiation and progression, where M2-polarized macrophages exert pivotal effects. NCAPD3 acts as an oncogenic driver in multiple tumors; how...
Objective To investigate the mechanism by which Notch1 induces M2 polarization of tumor-associated macrophages (TAMs) through regulation of the YAP/EZH2/JMJD3/PTEN/FOXD1/galectin-3/CD47 signaling pathway and its role in non-small cell lung cancer (NSCLC). Methods Bioinformatics analysis was utilized to identify Notch1...
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