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Immune escape plays a vital role in the development of liver cancer. The interaction between programmed death-ligand 1 (PD-L1) and programmed cell death-1 is a key mediator of cancer immune escape, which leads to the suppression of anticancer immunity and promotion of tumor progression. Hypoxia is a common phenomenon in the tumor microenvironment. Under hypoxic conditions, suppressive immune cells, such as regulatory T cells, myeloid-derived suppressor cells and M2 macrophages, are frequently recruited to tumor tissues to form the immunosuppressive microenvironment in liver cancer. These cells secrete cancer-promoting inflammatory cytokines, which activate the STAT3 and NF-κB signaling pathways. Recent studies have shown that STAT3 is associated with NF-κB and that these transcription factors are often co-activated to regulate tumor proliferation, survival, angiogenesis and invasion. The activation of STAT3 and NF-κB signaling pathways can directly and indirectly induce PD-L1 expression. Therefore, further understanding of the association between hypoxia and PD-L1 may help in the future treatment of liver cancer. The present review summarizes the recent progresses on PD-L1-mediated regulation and facilitation of liver cancer cell immune escape in response to hypoxia.

Role and mechanism of programmed death‑ligand�1 in hypoxia‑induced liver cancer immune escape (Review)