ArticleJournal for immunotherapy of cancer2026
Extracellular granzyme K enhances PD-L1 transcription and stability via F2RL1 activation to facilitate tumor immune evasion in lung adenocarcinoma.
Article in Journal for immunotherapy of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Post-Translational Modifications in Cancer-Associated CD8⁺ T-Cell Exhaustion: Mechanisms and Therapeutic Opportunities.International journal of biological sciences · 2026Review
- Metabolic dysfunction and GZMKFrontiers in immunology · 2026Review
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Authors and funding
11 authors.
Funding
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Abstract
backgroundGranzyme K (GZMK) is a serine protease known for its perforin-dependent cytotoxicity. However, the non-cytotoxic role of GZMK in lung adenocarcinoma (LUAD) remains largely elusive.
methodsMultiomics datasets were integrated to investigate the clinical relevance of GZMK and its association with programmed death-ligand 1 (PD-L1) in LUAD. Recombinant human GZMK (rhGzmK) was applied in tumor-CD8
resultsGZMK upregulated PD-L1 expression on tumor cells and enhanced PD-L1/PD-1 binding. Furthermore, GZMK promoted CD8
conclusionIn the absence of perforin, GZMK acquires an immunosuppressive function through F2RL1 activation on tumor cells, which in turn promotes the formation of an immune-suppressive niche. Accordingly, combined targeting of the GZMK/F2RL1 axis and the PD-1/PD-L1 pathway represents a promising synergistic strategy to overcome immune evasion in LUAD.
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