ArticleNature communications2023
TRABID inhibition activates cGAS/STING-mediated anti-tumor immunity through mitosis and autophagy dysregulation.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
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- Smyca-FOXM1 ribonucleoprotein complex promotes homologous recombination and tumor immune evasion to define a therapeutic target of triple-negative breast cancer.Journal of biomedical science · 2026Article
- Cathepsin L deletion enhances sensitivity to anticancer drugs through Parkin-mediated ubiquitination of Bcl-xL and USP53-induced Survivin destabilization.Cell death and differentiation · 2026Article
- ZRANB1 promotes cell proliferation and lymph node metastasis through SF3B3-mediated alternative splicing of CHEK2 in urothelial bladder cancer.Cell death & disease · 2026Article
- Nanomedicine leverages cuproptosis-mediated cGAS-STING activation to enhance antitumor immunity.Journal of nanobiotechnology · 2026Review
- The MAD2L1-FOXM1 axis negatively regulates CD4⁺ T cell and macrophages infiltration in lung adenocarcinoma.Discover oncology · 2026Article
- Wnt/β-Catenin-mTOR-autophagy crosstalk in breast cancer: context-dependent control of tumor progression, immune suppression, and therapeutic resistance.Frontiers in immunology · 2026Review
- PBLD Orchestrates the STING-Mediated Antiviral Immune Response and Autoimmune Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Methyltransferase-Like 3 Inhibition-Activated cGAS/STING Axis Enhances Immunotherapy and Poly(ADP-Ribose) Polymerase Inhibitor Sensitivity in Lung Adenocarcinoma.Research (Washington, D.C.) · 2026Article
- cGAS-STING and autophagy: crosstalk, molecular mechanisms, and targeted therapy.Archives of toxicology · 2026Review
- cGAS-STING and PANoptosis: Interplay, Underlying Mechanisms, and Therapeutic Targets.Drug design, development and therapy · 2026Review
- CircRNAAutophagy · 2025Article
- Article
- Research Progress on Polymer-Based Nanocarriers for Tumor-Targeted Delivery of Survivin siRNA.Polymers · 2025Review
- Targeting the interplay of cGAS-STING and ferroptosis by nanomedicine in the treatment of cancer.Journal of experimental & clinical cancer research : CR · 2025Review
- Unlocking the therapeutic potential of the STING signaling pathway in anti-tumor treatment.Clinical and experimental medicine · 2025Review
- Long-term SiNPs exposure induced genetic instability and malignant transformation via SQSTM1/p62-mediated autophagy dysfunction in lungs.Materials today. Bio · 2025Article
- cGAS, an innate dsDNA sensor with multifaceted functions.Cell insight · 2025Review
- Mitochondrial PTRH2 controls the deubiquitinase TRABID to regulate mt-ND5 stability and metabolism.PNAS nexus · 2025Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of tumor-intrinsic innate immunity has been a major strategy for improving immunotherapy. Previously, we reported an autophagy-promoting function of the deubiquitinating enzyme TRABID. Here, we identify a critical role of TRABID in suppressing anti-tumor immunity. Mechanistically, TRABID is upregulated in mitosis and governs mitotic cell division by removing K29-linked polyubiquitin chain from Aurora B and Survivin, thereby stabilizing the entire chromosomal passenger complex. TRABID inhibition causes micronuclei through a combinatory defect in mitosis and autophagy and protects cGAS from autophagic degradation, thereby activating the cGAS/STING innate immunity pathway. Genetic or pharmacological inhibition of TRABID promotes anti-tumor immune surveillance and sensitizes tumors to anti-PD-1 therapy in preclinical cancer models in male mice. Clinically, TRABID expression in most solid cancer types correlates inversely with an interferon signature and infiltration of anti-tumor immune cells. Our study identifies a suppressive role of tumor-intrinsic TRABID in anti-tumor immunity and highlights TRABID as a promising target for sensitizing solid tumors to immunotherapy.
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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 OpenQuestion graph.