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. Author manuscript; available in PMC: 2024 Oct 1.
Published in final edited form as: Gut. 2023 Jan 2;72(10):1942–1958. doi: 10.1136/gutjnl-2022-327924

Figure 11. A model depicting the anti-HCC role of miR-223 in blocking tumor hypoxia-driven PD-1/PD-L1 immunosuppression and angiogenesis.

Figure 11.

In chronic inflammation-associated HCC, the source of miR-223 in HCCs is likely transferred via the extracellular vesicles from myeloid cells including neutrophils and macrophages, which are enriched in adjacent tumor regions. MiR-223 directly inhibits Hif1a/HIF-1α in HCC cells and subsequently alters hypoxic tumor microenvironment, thereby limiting hypoxia-driven angiogenesis and immunosuppression. HIF-1α-mediated upregulation of CD39/CD73-adenosine pathway contributes to PD-1 and PD-L1 upregulation in immune cells, which is suppressed by miR-223.