ArticleActa pharmacologica Sinica2026
DNMT inhibition epigenetically restores the cGAS-STING pathway and activates RIG-I/MDA5-MAVS to enhance antitumor immunity.
Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Tumour-associated dsRNA accumulation and innate immune activation: mechanistic basis and therapeutic strategies.EBioMedicine · 2026Review
- Viral mimicry escape as a necessary feature of malignant transformation.Nature reviews. Cancer · 2026Review
- Tuning epigenetics to enhance cancer virotherapy.Acta pharmaceutica Sinica. B · 2026Review
- CDO1 as a prognostic biomarker and therapeutic target in gastric cancer: Mechanistic insights into the PI3K/AKT-THBS1 axis and epigenetic reactivation by decitabine.Clinical and translational medicine · 2026Article
- Review
- Targeting MORC2 activates transposable element-mediated viral mimicry and potentiates immune checkpoint blockade in triple-negative breast cancer.Molecular cancer · 2026Article
- Article
- Review
- Calibrating the RT-cGAS-STING axis to drive cold-to-hot tumor transformation: mechanistic foundations and translational strategies for combination with immunotherapy.Molecular cancer · 2026Review
- Loss of MicroRNA-29b promotes DNMT3b-mediated STING downregulation to attenuate radiotherapy-induced antitumor immunity in KRAS-mutated colorectal cancer.NPJ precision oncology · 2026Article
- Cell-type specific activation of the cGAS-STING pathway in tumor immunotherapy: mechanisms and therapeutic implications.Journal of translational medicine · 2026Review
- The cGAS-STING pathway in tumor immunity: dual roles, regulatory mechanisms, and precision therapeutic strategies.Frontiers in pharmacology · 2026Review
- Innate immune sensing via the cGAS-STING pathway restricts extrachromosomal DNA-driven tumorigenesis.bioRxiv : the preprint server for biology · 2026Article
- Targeting the cGAS-STING Pathway in Gastrointestinal Cancers: Modulating Tumor-associated Inflammation for Therapeutic Effect.Current drug targets · 2026Review
- Activation of endogenous retroviruses in tumor cells and their immunomodulatory mechanisms: from molecular basis to clinical translation.Frontiers in oncology · 2026Review
- Epigenetic regulatory mechanisms of autoimmune skin diseases: novel biomarkers and therapeutic prospects.Clinical epigenetics · 2025Review
- In Situ Vaccination by Tumor Ablation: Principles and Prospects for Systemic Antitumor Immunity.Vaccines · 2025Review
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12 authors.
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Abstract
The cGAS-STING cytosolic DNA-sensing pathway is a key mediator of the innate immune response and plays a crucial role in antitumor immunity. The expression of cGAS and STING is often suppressed in tumor cells, and reduced expression is associated with poor prognosis and inferior response to immunotherapy. In this study we systematically investigated the expression pattern of cGAS-STING pathway in tumors and its correlation with immunotherapy response. We showed that the expression of cGAS and STING was significantly decreased or undetectable in most breast cancer and murine tumor cell lines, while high cGAS and STING expression was associated with increased T cell infiltration, elevated PD-L1 and PD-1 levels, improved immunotherapy response and prolonged survival. In cGAS-STING-deficient MDA-MB-453 cells, DNMT inhibitor decitabine (DAC, 0.05-1 μM) dose-dependently restored the impaired pathway by reversing DNA methylation-mediated silencing. Furthermore, DAC combined with a chemotherapeutic agent cisplatin significantly enhanced the antitumor effect in MDA-MB-453 and MDA-MB-231 cells by activating the cGAS-STING pathway through cytoplasmic DNA accumulation. In addition, DNMT inhibition elevated intracellular dsRNA levels and activated the RIG-I/MDA5-MAVS pathway. These results suggest that DNMT inhibitors can epigenetically reprogram the cGAS-STING pathway, activate the RIG-I/MDA5-MAVS pathway, and in combination with chemotherapeutic agents, synergistically promote antitumor immunity. Together, this study identifies cGAS-STING as a potential predictor of immunotherapy response and highlights a novel therapeutic strategy for restoring innate immune function in cancer. Loss of cGAS-STING signaling in tumors impairs antitumor immunity and correlates with poor immunotherapy response. DNMT inhibition restores cGAS-STING pathway and concurrently activates the RIG-I/MDA5-MAVS signaling, synergistically enhancing immune infiltration and antitumor efficacy.
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