ArticleAmerican journal of cancer research2026
IL-23 promotes PD-L1 expression and tumor immune evasion via METTL16 pathway.
Article in American journal of cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Interleukin-23 (IL-23) is a pivotal cytokine implicated in tumor progression and immune evasion, yet its precise molecular mechanisms remain incompletely characterized. In this study, we elucidate that IL-23 upregulates METTL16, which in turn enhances PD-L1 expression and facilitates tumor immune escape. Integrated analysis of TCGA and GEO datasets revealed the co-upregulation of IL-23 and METTL16 in lung and colon carcinomas, both of which are correlated with poor clinical outcomes. Mechanistically, IL-23 induces METTL16 expression in cancer cells via JAK-STAT3 pathway-mediated transcriptional activation. Notably, METTL16 augments PD-L1 levels via an m6A-independent mechanism by directly binding to PD-L1 and impeding its SPOP-mediated ubiquitination and proteasomal degradation. In vivo, METTL16 promotes colon cancer xenograft growth while concurrently suppressing CD8
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