Coordinated Post-Transcriptional Regulation facilitates PD-L1 protein production and tumor immune suppression.

Cancer Lett 2026

Chen R, Rajasekaran S, Xing X, Zhang Q, Steele SM et al.

Abstract

PD-L1 drives T cell exhaustion and tumor immune evasion and is transcriptionally induced by immune cell-derived IFN-γ. Here, we find that the RNA-binding protein PUM1 recognizes a conserved 3’UTR motif in PD-L1 and is itself induced by IFN-γ. In PUM1-deficient cells, PD-L1 fails to accumulate with IFN-γ stimulation, revealing that IFN-γ also regulates PD-L1 through PUM1-mediated post-transcriptional mechanisms. Mechanistically, we identify HNRNPA2B1 as a direct competitor of PUM1 for PD-L1 mRNA binding, thereby controlling RNA stability and protein expression. In syngeneic colon cancer models, PUM1 deficiency reduces PD-L1, slows tumor growth, and enhances CD8

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