ArticleNature immunology2022
Type I IFNs promote cancer cell stemness by triggering the epigenetic regulator KDM1B.
Article in Nature immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 112 citations in OpenAlex.
- The immunology of human breast cancer.Nature reviews. Immunology · 2026Review
- CAFs shape the immunosuppressive microenvironment of pancreatic cancer through the Lin28b-STING Axis.Nature communications · 2026Article
- BRCA1 deficiency induces NFκB-dependent type-I interferon signaling in fallopian tube epithelial cells.Neoplasia (New York, N.Y.) · 2026Article
- Ecosystem-matched reprogramming of the tumor-immune microenvironment to overcome cancer immunotherapy resistance.Molecular cancer · 2026Review
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- Striking the right balance with type I interferon signalling in cancer.Nature reviews. Cancer · 2026Review
- Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma.Molecular oncology · 2026Article
- Identification and characterization of lncRNA-stemness-immune regulatory patterns.Briefings in bioinformatics · 2026Article
- Promotion of breast cancer by the DNPH1 enzyme.iScience · 2026Article
- Modifying Epigenetic Landscapes to Restore Immune Therapeutic Responses in Triple Negative Breast Cancer.Cancers · 2026Review
- Cancer and aging: complex associations and therapeutic targets.Molecular biomedicine · 2026Review
- Single-cell profiling of tumor lineage plasticity and the immune microenvironment in transformed small cell lung cancer.Journal of translational medicine · 2026Article
- Identifying the therapeutic potential of niclosamide in overcoming IFN-gamma dependent cancer immune evasion in the tumor microenvironment.Frontiers in immunology · 2026Article
- IFNβ-pSTAT1-IRF1 axis controls colorectal tumor development through induction of immunogenic Ly6CNeoplasia (New York, N.Y.) · 2026Article
- Epigenetic plasticity and chemoresistance in cancer: mechanisms, biomarkers, and translational opportunities for real-world evidence.Frontiers in cell and developmental biology · 2026Review
- Histone lysine demethylases in breast cancer: molecular mechanisms, biological functions, and therapeutic intervention.Molecular cancer · 2025Review
- A pan-cancer analysis of the oncogenic role of KIF13A in human tumors.Discover oncology · 2025Article
- NAT10-mediated ac4C modification of KDM1B drives osteoarthritis progression through epigenetic suppression of SOX9.Cellular and molecular life sciences : CMLS · 2025Article
- Drug-tolerant persister cells in cancer: bridging the gaps between bench and bedside.Nature communications · 2025Review
- The regulatory role and mechanism of energy metabolism and immune response in head and neck cancer.Genes & diseases · 2025Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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- Erratum issued
Authors and funding
43 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells (CSCs) are a subpopulation of cancer cells endowed with high tumorigenic, chemoresistant and metastatic potential. Nongenetic mechanisms of acquired resistance are increasingly being discovered, but molecular insights into the evolutionary process of CSCs are limited. Here, we show that type I interferons (IFNs-I) function as molecular hubs of resistance during immunogenic chemotherapy, triggering the epigenetic regulator demethylase 1B (KDM1B) to promote an adaptive, yet reversible, transcriptional rewiring of cancer cells towards stemness and immune escape. Accordingly, KDM1B inhibition prevents the appearance of IFN-I-induced CSCs, both in vitro and in vivo. Notably, IFN-I-induced CSCs are heterogeneous in terms of multidrug resistance, plasticity, invasiveness and immunogenicity. Moreover, in breast cancer (BC) patients receiving anthracycline-based chemotherapy, KDM1B positively correlated with CSC signatures. Our study identifies an IFN-I → KDM1B axis as a potent engine of cancer cell reprogramming, supporting KDM1B targeting as an attractive adjunctive to immunogenic drugs to prevent CSC expansion and increase the long-term benefit of therapy.
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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.