ArticleThe Journal of clinical investigation2018
STAT3/p53 pathway activation disrupts IFN-β-induced dormancy in tumor-repopulating cells.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 102 citations in OpenAlex.
- From paradox to target: IFN-β hijacks MEK signaling to drive a cell death-evading dormant phenotype in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Decoding the metabolic cipher of dormant cancer cells: molecular mechanisms and therapeutic potentials.Cell communication and signaling : CCS · 2026Review
- AhR-Siglec-15 axis regulates lysosomal Ca2+ release for sonic hedgehog medulloblastoma growth via TRPML1.Protein & cell · 2026Article
- Regulating the dormancy of cancer stem cells: a novel approach to preventing cancer relapse.Cell death & disease · 2026Review
- Gasdermin E-mediated lysosome-pore formation curbs pancreatic ductal adenocarcinoma via IFN-γ/IFN-β/TGF-β cocktail mRNA-LNP.Cellular & molecular immunology · 2026Article
- Immune Niche Formation Reveals Mechanisms of Tumor Dormancy and Targeting Opportunities.Research square · 2026Article
- PRMT3 Drives IDO1-Dependent Radioresistance and Immunosuppression by Promoting Kynurenine Metabolism in Non-Small Cell Lung Cancer.Cancer research · 2026Article
- RSL3 Promotes STAT3 Ubiquitination to Induce Autophagy and Apoptosis in PARPi-Resistant Breast Cancer Cells.Biomolecules · 2025Article
- Cross-talk between cancer-associated fibroblasts and dormant cancer cells: current status and promising therapeutic potential.Cancer cell international · 2025Review
- Macrophage regulation of tumor cell dormancy and the dormant niche: an overview in solid tumors.Cancer metastasis reviews · 2025Review
- Immune Niche Formation in Engineered Mouse Models Reveals Mechanisms of Tumor Dormancy.bioRxiv : the preprint server for biology · 2025Article
- Stanniocalcin-1 promotes temozolomide resistance of glioblastoma through regulation of MGMT.Scientific reports · 2024Article
- Advances in the molecular regulation mechanism of tumor dormancy and its therapeutic strategy.Discover oncology · 2024Review
- Sustained AhR activity programs memory fate of early effector CD8Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Dormancy of cutaneous melanoma.Cancer cell international · 2024Review
- EGFR core fucosylation, induced by hepatitis C virus, promotes TRIM40-mediated-RIG-I ubiquitination and suppresses interferon-I antiviral defenses.Nature communications · 2024Article
- Immune escape and metastasis mechanisms in melanoma: breaking down the dichotomy.Frontiers in immunology · 2024Review
- Aryl hydrocarbon receptor sulfenylation promotes glycogenolysis and rescues cancer chemoresistance.The Journal of clinical investigation · 2023Article
- Tumor cell-released kynurenine biases MEP differentiation into megakaryocytes in individuals with cancer by activating AhR-RUNX1.Nature immunology · 2023Article
- Aryl hydrocarbon receptor is a proviral host factor and a candidate pan-SARS-CoV-2 therapeutic target.Science advances · 2023Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
26 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dynamic interaction with the immune system profoundly regulates tumor cell dormancy. However, it is unclear how immunological cues trigger cancer cell-intrinsic signaling pathways for entering into dormancy. Here, we show that IFN-β treatment induced tumor-repopulating cells (TRC) to enter dormancy through an indolamine 2,3-dioxygenase/kynurenine/aryl hydrocarbon receptor/p27-dependent (IDO/Kyn/AhR/p27-dependent) pathway. Strategies to block this metabolic circuitry did not relieve dormancy, but led to apoptosis of dormant TRCs in murine and human melanoma models. Specifically, blocking AhR redirected IFN-β signaling to STAT3 phosphorylation through both tyrosine and serine sites, which subsequently facilitated STAT3 nuclear translocation and subsequent binding to the p53 promoter in the nucleus. Upregulation of p53 in turn disrupted the pentose phosphate pathway, leading to excessive ROS production and dormant TRC death. Additionally, in melanoma patients, high expression of IFN-β correlated with tumor cell dormancy. Identification of this mechanism for controlling TRC dormancy by IFN-β provides deeper insights into cancer-immune interaction and potential new cancer immunotherapeutic modalities.
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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.