ArticleCell death discovery2024
NAT10-mediated upregulation of GAS5 facilitates immune cell infiltration in non-small cell lung cancer via the MYBBP1A-p53/IRF1/type I interferon signaling axis.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Dark matter matters: from noncoding RNA regulation to cancer immunity.Oncoimmunology · 2026Review
- N-Acetyltransferase 10 (NAT10) at the crossroads of metabolism, immunology, and cancer biology.Cancer metastasis reviews · 2026Review
- Depletion of NAT10 in T cells attenuates metabolic dysfunction-associated steatohepatitis in mice.Hepatology communications · 2026Article
- NAT10-mediated acCellular & molecular biology letters · 2026Article
- Beyond miRNAs: exploratory profiling of PIWI-interacting RNAs and small nucleolar RNAs in non-small cell lung cancer-related malignant pleural effusions.Translational lung cancer research · 2026Article
- RNA N4-acetylcytidine modification in human cancers: from molecular function to oncogenic mechanisms.iScience · 2026Review
- The NAT10/acCell communication and signaling : CCS · 2026Review
- Non-Coding RNAs as key regulators of interferon signaling in cancer immunotherapy: mechanistic insights and clinical prospects.Clinical and experimental medicine · 2026Review
- Reprogramming Tumor-Associated Macrophages via Targeted NAT10 Inhibition to Enhance Colorectal Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- NAT10 as a central node in cancer biology: integrating epitranscriptomic regulation, metabolic reprogramming, and immune modulation.Frontiers in immunology · 2026Review
- Functional roles and mechanisms of NAT10-mediated RNA acFrontiers in cell and developmental biology · 2026Review
- N4-acetylcytidine modification bridges metabolic reprogramming and immune evasion in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- RNA modifications: roles in immune cell biology and tumor regulation.Cancer cell international · 2025Review
- Identification of the Role ofVeterinary sciences · 2025Article
- The function of NAT10-driven N4-acetylcytidine modification in cancer: novel insights and potential therapeutic targets.Cell & bioscience · 2025Review
- Integrating Single-Cell Transcriptomics and Machine Learning to Define an ac4C Gene Signature in Lung Adenocarcinoma.Thoracic cancer · 2025Article
- Immune evasion in cancer: mechanisms and cutting-edge therapeutic approaches.Signal transduction and targeted therapy · 2025Review
- Emerging role of N-acetyltransferase 10 in diseases: RNA ac4C modification and beyond.Molecular biomedicine · 2025Review
- LncRNAs and IgA nephropathy: underlying molecular pathways and clinical applications.Clinical and experimental medicine · 2025Review
- NAT10 Knockdown Improves Cisplatin Sensitivity in Non-Small Cell Lung Cancer by Inhibiting the TRIM44/PI3K/AKT Pathway.Thoracic cancer · 2025Article
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Authors and funding
15 authors.
Funding
Abstract
Interactions of tumor cells with immune cells in the tumor microenvironment play an important role during malignancy progression. We previously identified that GAS5 inhibited tumor development by suppressing proliferation of tumor cells in non-small cell lung cancer (NSCLC). Herein, we discovered a tumor-suppressing role for tumor cell-derived GAS5 in regulating tumor microenvironment. GAS5 positively coordinated with the infiltration of macrophages and T cells in NSCLC clinically, and overexpression of GAS5 promoted macrophages and T cells recruitment both in vitro and in vivo. Mechanistically, GAS5 stabilized p53 by directly binding to MYBBP1A and facilitating MYBBP1A-p53 interaction, and enhanced p53-mediated transcription of IRF1, which activated type I interferon signaling and increased the production of downstream CXCL10 and CCL5. We also found that activation of type I interferon signaling was associated with better immunotherapy efficacy in NSCLC. Furthermore, the stability of GAS5 was regulated by NAT10, the key enzyme responsible for N4-acetylcytidine (ac4C) modification, which bound to GAS5 and mediated its ac4C modification. Collectively, tumor cell-derived GAS5 could activate type I interferon signaling via the MYBBP1A-p53/IRF1 axis, promoting immune cell infiltration and potentially correlating with immunotherapy efficacy, which suppressed NSCLC progression. Our results suggested GAS5 as a promising predictive marker and potential therapeutic target for combination therapy in NSCLC. A schematic diagram demonstrating the regulatory effect of GAS5 on immune cell infiltration by activating type I interferon signaling via MYBBP1A-p53/IRF1 axis in non-small cell lung cancer. IFN, interferon.
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Registered trials
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