ArticleExperimental & molecular medicine2020
The cGAS/STING/TBK1/IRF3 innate immunity pathway maintains chromosomal stability through regulation of p21 levels.
Article in Experimental & molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 110 citations in OpenAlex.
- The Role of cGAS-STING-Driven PANoptosis in Neurodegenerative Diseases and Therapeutic Prospects.Cells · 2026Review
- Clinical and immunological characterization of a child with a homozygous TBK1 kinase-domain truncation.Immunologic research · 2026Article
- Immune pathway activation in gastric cancers with LINE-1 retrotransposon overexpression and homologous recombination deficiency.Experimental & molecular medicine · 2026Article
- Can Disruption of Circadian Rhythms Be Linked to Radiation-Induced Acute Myeloid Leukaemia?Cancers · 2026Review
- Ciliated Cells Drive Critical STING-Mediated Tumor Suppression in the Fallopian Tube Epithelium.Cancer research · 2026Article
- Chlamydia trachomatis orchestrates multifaceted host cell manipulation for immune evasion.Communications biology · 2026Review
- Targeting Ferroptosis to Overcome Radioresistance and Enhance Immunotherapy in Colorectal Cancer.Cells · 2026Review
- Review
- The cGAS-STING pathway in cancer: friend or foe.Cell death & disease · 2026Review
- SFPQ directs histone H3.3 deposition to R-loops in DNA repeats to protect genome stability.Nature communications · 2026Article
- Anticodon-edited transfer RNAs (ACE-tRNAs) encoded as therapeutic nonviral minimal DNA vectors.Nucleic acids research · 2026Article
- An ultrasmall core-shell silica nanoparticle improves antitumour immunity and survival by remodelling suppressive melanoma microenvironments.Nature nanotechnology · 2026Article
- Tetrandrine enhances anti-PD-1 immunotherapeutic efficacy for hepatocellular carcinoma by activating STING/TBK1/IRF3 pathway.Frontiers in immunology · 2026Article
- Article
- Article
- ERBB2 signaling drives immune cell evasion and resistance against immunotherapy in small cell lung cancer.Nature communications · 2025Article
- Immune Modulation in Cancer: The Role of Tumor-Treating Fields (TTFields).Current protocols · 2025Review
- HSV-1 US3: A Master Mimic Hijacking Host Kinase Networks for Viral Dominance.Journal of medical virology · 2025Review
- Genome instability and crosstalk with the immune response.Genome medicine · 2025Review
- Roles of Autophagy and Oxidative Stress in Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2025Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Chromosomal instability (CIN) in cancer cells has been reported to activate the cGAS-STING innate immunity pathway via micronuclei formation, thus affecting tumor immunity and tumor progression. However, adverse effects of the cGAS/STING pathway as they relate to CIN have not yet been investigated. We addressed this issue using knockdown and add-back approaches to analyze each component of the cGAS/STING/TBK1/IRF3 pathway, and we monitored the extent of CIN by measuring micronuclei formation after release from nocodazole-induced mitotic arrest. Interestingly, knockdown of cGAS (cyclic GMP-AMP synthase) along with induction of mitotic arrest in HeLa and U2OS cancer cells clearly resulted in increased micronuclei formation and chromosome missegregation. Knockdown of STING (stimulator of interferon genes), TBK1 (TANK-binding kinase-1), or IRF3 (interferon regulatory factor-3) also resulted in increased micronuclei formation. Moreover, transfection with cGAMP, the product of cGAS enzymatic activity, as well as add-back of cGAS WT (but not catalytic-dead mutant cGAS), or WT or constitutively active STING (but not an inactive STING mutant) rescued the micronuclei phenotype, demonstrating that all components of the cGAS/STING/TBK1/IRF3 pathway play a role in preventing CIN. Moreover, p21 levels were decreased in cGAS-, STING-, TBK1-, and IRF3-knockdown cells, which was accompanied by the precocious G2/M transition of cells and the enhanced micronuclei phenotype. Overexpression of p21 or inhibition of CDK1 in cGAS-depleted cells reduced micronuclei formation and abrogated the precocious G2/M transition, indicating that the decrease in p21 and the subsequent precocious G2/M transition is the main mechanism underlying the induction of CIN through disruption of cGAS/STING signaling.
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