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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: Exosomal cargos-mediated metabolic reprogramming in tumor microenvironment

Fig. 5

The mechanism of tumor-serected exosomal cargos regulate metabolic reprogramming of immune cells. Tumor cells-secreted exosomal miR-451 can target AMPK to activate the mTOR pathway and promote Th17 polarized differentiation of T cells through glucose deprivation. Cervical squamous carcinoma-derived exosomal miR-142-5p can target ARID2 to inhibit DNMT1 recruitment to the INF-γ promoter, leading to up-regulation of IDO, thereby suppressing and exhausting CD8 + T cells. Prostate cancer-derived exosomal Rab27a can promote CD73 expression in DCs, which hydrolyzes AMP to adenosine and inhibits the production of TNFα and IL-1L in an ATP-dependent manner, resulting in functional inhibition of DCs. Hypoxia-induced exosomal let-7a can inhibit the insulin-AKT-mTOR pathway and induce M2-polarized TAMs by enhancing OXPHOS. Lung cancer cell-secreted exosomal PKM2 can activate the AMPK pathway to induce M2-polarized TAMs, in which exosome-mediated glycolytic remodeling may play a role. HNSCC cells-derived exosomal metabolite adenosine can induce A2BR-mediated M2-polarized TAMs

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