Fig. 8

Schematic representation of spermine-mediated PD-L1 expression and glycosylation in HCC. Spermine triggers Akt-dependent β-catenin phosphorylation at Ser552 through acting on CaSR, phosphorylated β-catenin then translocates into the nucleus where it transcriptionally activates PD-L1 and STT3A expression by binding to their promoter regions. On the other hand, STT3A stabilizes PD-L1 by modulating protein N-glycosylation, resulting in the suppression of cytotoxic T cell activity in the tumor microenvironment