ArticleScientific reports2020
The mechanism of how CD95/Fas activates the Type I IFN/STAT1 axis, driving cancer stemness in breast cancer.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- RUNX1 restrains STAT1-GITRL signaling to shape an immunosuppressive CRC microenvironment.Cell death discovery · 2026Article
- SNP's use as a potential chemotoxicity stratification tool in breast cancer: from bench to clinic.Functional & integrative genomics · 2025Review
- Review
- FAS gene expression, prognostic significance and molecular interactions in lung cancer.Frontiers in oncology · 2024Article
- Analysis of the role of dihydromyricetin derived from vine tea (Oncology research · 2024Article
- Regulation of cellular senescence by innate immunity.Biophysics reports · 2023Article
- DDX18 drives tumor immune escape through transcription-activated STAT1 expression in pancreatic cancer.Oncogene · 2023Article
- Immune system and tumor microenvironment in early-stage breast cancer: different mechanisms for early recurrence after mastectomy and chemotherapy on ductal and lobular types.F1000Research · 2023Article
- STAT family of transcription factors in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Seminars in cancer biology · 2022Review
- Targeting histone methylation to reprogram the transcriptional state that drives survival of drug-tolerant myeloid leukemia persisters.iScience · 2022Article
- FAS receptor regulates NOTCH activity through ERK-JAG1 axis activation and controls oral cancer stemness ability and pulmonary metastasis.Cell death discovery · 2022Article
- Fas and Fas ligand are highly expressed in lymphocytes from cervical intraepithelial neoplasia and cervical cancer patients: A possible role for immune escaping.Iranian journal of basic medical sciences · 2022Article
- CD95/Fas protects triple negative breast cancer from anti-tumor activity of NK cells.iScience · 2021Article
- TNF-α synergises with IFN-γ to induce caspase-8-JAK1/2-STAT1-dependent death of intestinal epithelial cells.Cell death & disease · 2021Article
- Induction of interferon-β and interferon signaling by TRAIL and Smac mimetics via caspase-8 in breast cancer cells.PloS one · 2021Article
- CD95L and Anti-Tumor Immune Response: Current Understanding and New Evidence.Cancer management and research · 2021Article
- FasL (rs763110) gene polymorphism is not associated with susceptibility to rheumatoid arthritis in Croatian population.Croatian medical journal · 2020Article
- Type I interferons and related pathways in cell senescence.Aging cell · 2020Review
- Stress Management: Death Receptor Signalling and Cross-Talks with the Unfolded Protein Response in Cancer.Cancers · 2020Review
- Caspase-2 Substrates: To Apoptosis, Cell Cycle Control, and Beyond.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
CD95/Fas is an apoptosis inducing death receptor. However, it also has multiple nonapoptotic activities that are tumorigenic. Chronic stimulation of CD95 on breast cancer cells can increase their cancer initiating capacity through activation of a type I interferon (IFN-I)/STAT1 pathway when caspases are inhibited. We now show that this activity relies on the canonical components of the CD95 death-inducing signaling complex, FADD and caspase-8, and on the activation of NF-κB. We identified caspase-2 as the antagonistic caspase that downregulates IFN-I production. Once produced, IFN-Is bind to their receptors activating both STAT1 and STAT2 resulting in upregulation of the double stranded (ds)RNA sensor proteins RIG-I and MDA5, and a release of a subset of endogenous retroviruses. Thus, CD95 is part of a complex cell autonomous regulatory network that involves activation of innate immune components that drive cancer stemness and contribute to therapy resistance.
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