ArticleJournal for immunotherapy of cancer2022
Z-DNA enhances immunotherapy by triggering death of inflammatory cancer-associated fibroblasts.
Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Z-Nucleic Acid-Binding Protein (ZBP)1 (DAI/DLM1) Regulation in Antiviral Cell Death Pathways.Pathogens (Basel, Switzerland) · 2026Review
- Formation and biological implications of Z-DNA.Trends in genetics : TIG · 2026Review
- PANoptosis as a Two-Edged Sword in Colorectal Cancer: A Pathogenic Mechanism and Therapeutic Opportunity.Cells · 2025Review
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- Article
- Single-cell programmed cell death regulator patterns guide intercellular communication of cancer-associated fibroblasts that contribute to colorectal cancer progression.Translational cancer research · 2025Article
- Cancer-associated fibroblasts: dual roles from senescence sentinels to death regulators and new dimensions in therapy.Frontiers in immunology · 2025Review
- Influential upregulation of KCNE4: Propelling cancer associated fibroblasts-driven colorectal cancer progression.Cancer cell international · 2024Article
- Apoptosis dysfunction: unravelling the interplay between ZBP1 activation and viral invasion in innate immune responses.Cell communication and signaling : CCS · 2024Review
- Z-form nucleic acid-binding protein 1 (ZBP1) as a sensor of viral and cellular Z-RNAs: walking the razor's edge.Current opinion in immunology · 2023Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-associated fibroblasts (CAFs) are a heterogeneous population of cells. At one end of the spectrum are alpha-smooth muscle actin expressing myoCAFs (myofibroblast CAFs) and at the other end are the interferon (IFN) and Janus Kinase/Signal Transducer and Activator of Transcription responsive iCAFs (inflammatory CAFs). Both types of CAFs promote tumor growth. While myoCAFs foster immune exclusion and limit tumor spread, iCAFs create a highly immunosuppressive environment and foster the seeding of distant metastases. However, iCAFs also represent a tumor vulnerability. They are competent to undergo necroptosis, a highly immunogenic form of cell death that is triggered when Z-DNA or Z-RNA (collectively called ZNA) is sensed by the IFN-induced ZNA binding protein 1 (ZBP1). The sequestering of ZNA ligands by the p150 isoform of the double-stranded RNA-specific deaminase ADAR1 protects iCAFs from cell death. ZBP1-dependent necroptosis in iCAFs can be triggered by administering an orally available small molecule that generates sufficient amounts of ZNA to bypass ADAR1 inhibition. The therapeutic approach of targeting Z-prone sequences (called flipons) is agnostic to the mutations driving cancer progression. By exploiting the tumor vulnerability posed by expression of ZBP1-dependent immunogenic cell death pathways in iCAFs, flipon therapeutics offer new hope for improved clinical outcomes.
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