ArticleCancer letters2026
Coordinated post-transcriptional regulation facilitates PD-L1 protein production and tumor immune suppression.
Article in Cancer letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The identification of growth-promoting lncRNAs in oral cavity squamous cell carcinoma.Non-coding RNA research · 2026Article
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16 authors.
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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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