miR-802 has been reported to be dysregulated in multiple tumors and contribute to tumor progression. However, its role in HCC was still largely unknown. The aim of this study is to investigate the function and mechanism of miR-802 in HCC progression. The results showed that miR-802 was upregulated in the peripheral blood and tumor tissue of HCC patients, and high levels of blood miR-802 predicted poor prognosis. miR-802 had no effect on the proliferation and migration of HCC cell lines. Interestingly, the levels of CD8/CD28 and regulated in development and DNA damage response 1 (REDD1) were declined along with the upregulation of miR-802 in vivo. Hence, it is speculated that miR-802 participated in the regulation of T-cell function in HCC patients. Furthermore, we demonstrated that mir-802 directly targets REDD1 and inhibited its expression. miR-802 increased the expression of programmed cell death protein 1 (PD-1) and decreased the expression of interferon-γ (IFN-γ) and CD8+CD28+ T-cell number. In conclusion, miR-802 was involved in T-cell exhaustion through posttranscriptionally suppressing REDD1, which might offer the suppressive effect of miR-802 on HCC progression.

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