These findings illustrated that circPRDM4 promoted immune escape of HCC cells by facilitating the recruitment of HIF-1alpha onto the promoter of CD274 under hypoxia, thereby inhibiting CD8+ T cell infiltration in the tumor microenvironment.
Hypoxia-associated circPRDM4 promotes immune escape via HIF-1alpha regulation of PD-L1 in hepatocellular carcinoma.