ArticleCancer research2026
PRMT3 Drives IDO1-Dependent Radioresistance and Immunosuppression by Promoting Kynurenine Metabolism in Non-Small Cell Lung Cancer.
Article in Cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Spontaneous Intracellular Formation of Covalent Organic Frameworks via Enzyme-Initiated Cascade Reactions to Boost Cancer Radiotherapy.Journal of the American Chemical Society · 2026Article
- Radiosensitivity Prediction of Tumor Patient Based on Deep Fusion of Pathological Images and Genomics.Bioengineering (Basel, Switzerland) · 2026Article
- Editorial: Cancer cell metabolism and tumor microenvironment remodel.Frontiers in genetics · 2026Article
- PRMT3 in cancer: arginine methylation as a driver of tumor metabolism, immune evasion, and therapeutic resistance.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Radioresistance is one of the primary causes of treatment failure in non-small cell lung cancer. In this study, we identified protein arginine methyltransferase-3 (PRMT3) within tumors as a critical mediator impairing both radiotherapy sensitivity and T-cell antitumor activity. In tumor cells, PRMT3 mediated arginine methylation of transcription factor TFAP2A, enhancing its binding to the indoleamine 2,3-dioxygenase 1 (IDO1) promoter. Methylated TFAP2A exhibited a prolonged half-life, increased nuclear localization, and enhanced dimer formation, which ultimately led to heightened IDO1 expression that enhanced synthesis of kynurenine (Kyn). The elevated Kyn production boosted radioresistance in tumor cells and suppressed the infiltration and function of CD8+ T cells by activating aryl hydrocarbon receptors. Interestingly, combined pharmacologic inhibition of PRMT3 and IDO1 effectively disrupted the TFAP2A-IDO1-Kyn axis, overcoming radioresistance, activating antitumor immunity, and ultimately eradicating tumors. In conclusion, these findings delineate PRMT3-mediated Kyn metabolism as a mechanism of radioresistance and immune evasion in non-small cell lung cancer, offering valuable insights for potential interventions for treating patients with lung cancer. SIGNIFICANCE: PRMT3 orchestrates metabolic reprogramming in non-small cell lung cancer through a TFAP2A-IDO1 pathway that stimulates kynurenine synthesis to promote radioresistance and immunosuppression, highlighting this axis as a putative therapeutic target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.