ArticleJournal for immunotherapy of cancer2025
Targeting pyroptosis reverses KIAA1199-mediated immunotherapy resistance in colorectal cancer.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Single-cell and spatial transcriptomics reveal lactate-active epithelial-immune cell crosstalk that reprograms the immune microenvironment in colorectal cancer.Translational oncology · 2026Article
- Pyroptosis as a double-edged sword in colorectal cancer: Molecular mechanisms and therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2026Review
- Hepatocytes functionally reprogrammed by KIAA1199-high colorectal cancer cells favour the accumulation of pro-metastatic Egr1Nature communications · 2026Article
- The molecular mechanisms of pyroptosis and its implications in tumor immunotherapy.Molecular cancer · 2026Review
- The chromosomal instability associated gene C2orf76 exerts dual roles in colorectal cancer through pyroptosis and chemotherapy response.Frontiers in oncology · 2026Article
- Engineering a drug-inducible pyroptosis platform enables precise tumor suppression in colorectal cancer.Synthetic and systems biotechnology · 2025Article
- Targeting pyroptosis for cancer immunotherapy: mechanistic insights and clinical perspectives.Molecular cancer · 2025Review
- KIAA1199: A Novel Regulator of Chemoresistance in Human Cancer Cells.Cancer control : journal of the Moffitt Cancer CenterReview
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13 authors.
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Abstract
backgroundDespite advancements in treatment modalities, several patients with colorectal cancer (CRC) remain unresponsive to immune checkpoint inhibitor therapy. Pyroptosis, an inflammatory programmed cell death process, holds substantial promise for tumor immunotherapy. In this study, we explored the use of pyroptosis to overcome immunotherapy resistance in CRC.
methodsWe used a pyroptosis-related gene panel to construct an immunotherapy efficacy evaluation model and validated its performance by immunohistochemical staining of CRC patient samples. Pyroptosis and its underlying mechanisms were examined both in vitro and in vivo using PCR, western blotting, lactate dehydrogenase release assay, ELISA, co-immunoprecipitation, immunohistochemistry, fluorescence cell assays, microscopic imaging, flow cytometry analysis and bioinformatics approaches.
resultsWe established a model to define high or low levels of pyroptosis in CRC, revealed that low pyroptosis led to immunotherapy resistance, and identified KIAA1199 as a characteristic protein of low pyroptosis CRC. We further demonstrated that KIAA1199 contributes to low pyroptosis, resulting in resistance to immunotherapy. Mechanistically, KIAA1199 bound to and stabilized DNA methyltransferase-1 (DNMT1), thereby inhibiting GSDME-mediated pyroptosis. Importantly, our study highlighted that decitabine reversed KIAA1199-mediated immunotherapy resistance by enhancing pyroptosis to restore IL-1B release and CD8
conclusionsWe found a critical role of KIAA1199 in promoting immunotherapy resistance by suppressing pyroptosis via the DNMT1/GSDME pathway in CRC. Decitabine has emerged as a promising therapeutic agent for reversing KIAA1199-mediated immunotherapy resistance by enhancing pyroptosis. Our findings provide valuable insights for enhancing the efficacy of immunotherapy in patients with CRC who exhibit resistance to conventional immunotherapy approaches.
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