ArticleCell communication and signaling : CCS2022
ARID1A deficiency reverses the response to anti-PD(L)1 therapy in EGFR-mutant lung adenocarcinoma by enhancing autophagy-inhibited type I interferon production.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 13 citations in OpenAlex.
- ARID1A regulates colorectal cancer metastasis through the AKT/mTOR/p70S6K pathway.Translational oncology · 2026Article
- Histone Methylation and Chromatin Remodeling in Non-Small Cell Lung Cancer: Mechanisms of Oncogenesis and Emerging Therapeutic Strategies.Biomedicines · 2026Review
- Tumor cell intrinsic mechanisms of immune escape.Cell communication and signaling : CCS · 2026Review
- [Heterogeneity of Response to PD-1/PD-L1 Inhibitors in Elderly Patients with Advanced NSCLC under the Background of Immunosenescence and Intervention Strategies].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- Efficacy and mechanisms of immune checkpoint inhibitors in late-stage EGFR-mutated non-small cell lung cancer following targeted therapy resistance.Frontiers in immunology · 2026Review
- Epigenetic and metabolic plasticity of tumor cells in immunotherapy resistance.Frontiers in immunology · 2026Review
- ARID1A and Its Impact Across the Hallmarks of Cancer.International journal of molecular sciences · 2025Review
- Autophagy in tumor immune escape and immunotherapy.Molecular cancer · 2025Review
- Possible new mechanisms of primary drug resistance in NSCLC with EGFR mutation treated with Osimertinib.IUBMB life · 2025Article
- A cohort-based multi-omics identifies nuclear translocation of eIF5B /PD-L1/CD44 complex as the target to overcome Osimertinib resistance of ARID1A-deficient lung adenocarcinoma.Experimental hematology & oncology · 2025Article
- Potential role of lactylation in intrinsic immune pathways in lung cancer.Frontiers in pharmacology · 2025Review
- Development and validation of an ARID1A-related immune genes risk model in evaluating prognosis and immune therapeutic efficacy for gastric cancer patients: a translational study.Frontiers in immunology · 2025Article
- SMARCA4 mutations and expression in lung adenocarcinoma: prognostic significance and impact on the immunotherapy response.FEBS open bio · 2024Article
- Chromatin modifiers in human disease: from functional roles to regulatory mechanisms.Molecular biomedicine · 2024Review
- Targeting MDM2 in malignancies is a promising strategy for overcoming resistance to anticancer immunotherapy.Journal of biomedical science · 2024Review
- Programmed cell death in tumor immunity: mechanistic insights and clinical implications.Frontiers in immunology · 2023Review
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7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionEGFR mutations in non-small cell lung cancer (NSCLC) are associated with a poor response to immune checkpoint inhibitors (ICIs), and only 20% of NSCLC patients harboring EGFR mutations benefit from immunotherapy. Novel biomarkers or therapeutics are needed to predict NSCLC prognosis and enhance the efficacy of ICIs in NSCLC patients harboring EGFR mutations, especially lung adenocarcinoma (LUAD) patients, who account for approximately 40-50% of all NSCLC cases.
methodsAn ARID1A-knockdown (ARID1A-KD) EGFR-mutant LUAD cell line was constructed using lentivirus. RNA-seq and mass spectrometry were performed. Western blotting and IHC were used for protein expression evaluation. Effects of 3-MA and rapamycin on cells were explored. Immunofluorescence assays were used for immune cell infiltration examination.
resultsARID1A expression was negatively associated with immune cell infiltration and immune scores for ICIs in LUAD with EGFR mutations. In vitro experiments suggested that ARID1A-KD activates the EGFR/PI3K/Akt/mTOR pathway and inhibits autophagy, which attenuates the inhibition of Rig-I-like receptor pathway activity and type I interferon production in EGFR-mutant LUAD cells. In addition, 3-MA upregulated production of type I interferon in EGFR-mutant LUAD cells, with an similar effect to ARID1A-KD. On the other hand, rapamycin attenuated the enhanced production of type I interferon in ARID1A-KD EGFR-mutant LUAD cells. ARID1A function appears to influence the tumor immune microenvironment and response to ICIs.
conclusionARID1A deficiency reverses response to ICIs in EGFR-mutant LUAD by enhancing autophagy-inhibited type I interferon production. Video Abstract.
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