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mTORC2 regulates lipid metabolism-driven TAMs via the PPAR-γ/CD36 pathway to promote liposarcoma progression
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DOI：10.1080/21623945.2026.2665903.png)
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Abstract
En 中文
Tumour-associated macrophages (TAMs) exert a pivotal function in tumour progression, and M2-type TAMs are closely linked to tumour-promoting functions. Mechanistic target of rapamycin complex 2 (mTORC2) may mediate TAM polarization and subsequent tumour development, yet their roles in liposarcoma (LPS) remain unclear. Macrophage polarization was assessed via flow cytometry for CD206. Western blot for Arg-1, Rictor, PPAR-γ, CD36, ACSL1 and CPT2, qPCR for IL-10, Arg-1 and Ym1, and ELISA for IL-10 secretion. Fatty acid metabolism was evaluated using free fatty acid (FFA) uptake assays and Oil Red O staining for intracellular lipid droplets. A Transwell assay was established to assess the effect of treated macrophages on LPS cell biology, and EdU assays were used for proliferation assessment. Transwell migration and invasion assays were utilized for assessing cellular motility. IL-4 induced RAW264.7 macrophages to undergo M2 polarization, characterized by upregulated CD206, Arg-1, and IL-10. During this process, mTORC2 was activated, promoting FFA uptake, lipid droplet accumulation, and fatty acid oxidation via the PPAR-γ/CD36 axis. Co-culture experiments showed that IL-4-polarized M2 macrophages enhanced LPS cell proliferation, migration, and invasion; these effects were inhibited by JR-AB2-011 and restored by LPA, confirming mTORC2-PPAR-γ/CD36-mediated TAMs drive LPS progression. mTORC2 regulates M2 TAM polarization and metabolic reprogramming via the PPAR-γ/CD36 pathway, thereby promoting LPS cell proliferation, migration, and invasion.
Keywords:
mTORC2
tumour-associated macrophages
liposarcoma
fatty acid metabolism
PPAR-γ/CD36 pathway
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