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Figure 1. Representative examples of exosome-mediated intercellular communication within the hypoxic TME driving cancer progression, chemoresistance, and immune suppression. (1) Cancer proliferation: Hypoxic cancer-secreted exosomes were enriched with miRNAs supporting cell survival (e.g., miR-210) in the neighboring cancer cells. (2) Drug resistance: Numerous ncRNAs (e.g., linc-RoR and miR-21) were transferred via exosomes from hypoxic and resistant cancer cells to sensitive cells and induced drug resistance. (3) Migration and invasion: exosomes containing various ncRNAs (including lncRNA UCA1 and miR-193-3p) facilitate cancer–cancer or cancer–stromal intercellular communication to stimulate migration and invasion by modulating EMT. (4) Angiogenesis: ncRNAs (including miR-23a and lncRNA UCA1) were enriched in the exosomes secreted from hypoxic tumor cells to promote tumor vascular endothelial cell proliferation and angiogenesis in HIF-1α-dependent or -independent pathway. (5) Immune suppression: Exosomes enriched with miRNAs (e.g., miR-23a and let-7a) and other immunosuppressive molecules (e.g., PD-L1 and TGF-β1) were secreted from hypoxic tumors to promote an immunosuppressive TME. TME: Tumor microenvironment.