ArticleCancer research2021
Targeting DDX3X Triggers Antitumor Immunity via a dsRNA-Mediated Tumor-Intrinsic Type I Interferon Response.
Article in Cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Editing regulatory network in non-small cell lung cancer: implications for immunity and metastasis.Human genomics · 2026Article
- Identification of highly immunogenic endogenous dsRNAs from cellular MDA5 filaments.bioRxiv : the preprint server for biology · 2026Article
- RNA-binding proteins and ribonucleoproteins as determinants of immunity.Nature reviews. Immunology · 2026Review
- Human lncRNAProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Inducing tumor-intrinsic innate immune response to break cancer immunotherapy resistance.Frontiers in medicine · 2026Review
- Orchestrating innate immunity through RNA editing and helicase activity: ADAR1, dsRNA sensors, and tumor immune evasion.Frontiers in cell and developmental biology · 2026Review
- RNA binding protein DDX3X drives pancreatic cancer progression via the TLE2-MYL9 axis.Science advances · 2025Article
- ADAR1-mediated RNA editing in breast cancer: molecular mechanisms and therapeutic implications.Medical oncology (Northwood, London, England) · 2025Review
- Review
- Adar contributes to genome integrity by regulating R-loop homeostasis in Drosophila.BMC biology · 2025Article
- Inhibition of tumor-intrinsic NAT10 enhances antitumor immunity by triggering type I interferon response via MYC/CDK2/DNMT1 pathway.Nature communications · 2025Article
- DDX3X Activates Chondrocyte Pyroptosis to Promote Osteoarthritis Progression.Cell biochemistry and biophysics · 2025Article
- Neutrophils physically interact with tumor cells to form a signaling niche promoting breast cancer aggressiveness.Nature cancer · 2025Article
- The Gender-Biased Differential Effect ofCancers · 2025Article
- Exploring viral mimicry combined with epigenetics and tumor immunity: new perspectives in cancer therapy.International journal of biological sciences · 2025Review
- Immunomodulatory role of RNA modifications in sex hormone-dependent cancers.Frontiers in immunology · 2025Review
- The role of type I interferon signaling in myeloid anti-tumor immunity.Frontiers in immunology · 2025Review
- RNA helicases DDX3X and DDX3Y form nanometer-scale RNA-protein clusters that support catalytic activity.Current biology : CB · 2024Article
- Article
- Suppression of double-stranded RNA sensing in cancer: molecular mechanisms and therapeutic potential.Biochemical Society transactions · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Induction of nucleic acid sensing-mediated type I interferon (IFN) has emerged as a novel approach to activate the immune system against cancer. Here we show that the depletion of DEAD-box RNA helicase 3X (DDX3X) triggers a tumor-intrinsic type I IFN response in breast cancer cells. Depletion or inhibition of DDX3X activity led to aberrant cytoplasmic accumulation of cellular endogenous double-stranded RNAs (dsRNA), which triggered type I IFN production through the melanoma differentiation-associated gene 5 (MDA5)-mediated dsRNA-sensing pathway. Furthermore, DDX3X interacted with dsRNA-editing ADAR1 and dual depletion of DDX3X and ADAR1 synergistically activated the cytosolic dsRNA pathway in breast cancer cells. Loss of DDX3X in mouse mammary tumors enhanced antitumor activity by increasing the tumor-intrinsic type I IFN response, antigen presentation, and tumor infiltration of cytotoxic T and dendritic cells. These findings may lead to the development of a novel therapeutic approach for breast cancer by targeting DDX3X in combination with immune-checkpoint blockade. SIGNIFICANCE: This study elucidates the novel role of DDX3X in regulating endogenous cellular dsRNA homeostasis and type I IFN signaling in breast cancer. GRAPHICAL ABSTRACT: http://cancerres.aacrjournals.org/content/canres/81/13/3607/F1.large.jpg.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.