ArticleEBioMedicine2016
Upregulated LINE-1 Activity in the Fanconi Anemia Cancer Susceptibility Syndrome Leads to Spontaneous Pro-inflammatory Cytokine Production.
Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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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.
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Who cites it
73 citing papers in PubMed, 103 citations in OpenAlex.
- Review
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- Integrative proteomics defines FANCA as a multifunctional hub linking DNA repair to translation.iScience · 2026Article
- Activation of transposable elements is linked to a region- and cell type-specific interferon response in Parkinson's disease.Science advances · 2026Article
- SIRT1 Silences L1 Retrotransposons by Stabilizing Heterochromatin-Modifying Complexes.Aging cell · 2026Article
- Evolutionary conservation analysis reveals a primordial function of STING as a regulator of lipid metabolism via FADS2.Nature communications · 2026Article
- Host-transposable element coexistence: a matter of resistance, tolerance and trade-off.The EMBO journal · 2026Review
- Telomere Crisis Shapes Cancer Evolution.Cold Spring Harbor perspectives in biology · 2026Review
- The tight bond between Fanconi anemia and aging.Frontiers in aging · 2026Review
- Negative regulators antagonizing antitumor innate immune pathways in lung cancer immune evasion.Frontiers in immunology · 2026Review
- The fetal exposome: cellular and epigenetic programming of neonatal immune function.Frontiers in immunology · 2026Review
- The methyl-CpG-binding protein 2 inhibits cGAS-associated signaling.Nature communications · 2025Article
- Genome instability and crosstalk with the immune response.Genome medicine · 2025Review
- Antagonistic regulation of LINE-1/Alu elements and their repressor APOBEC3B in cellular senescence.Mobile DNA · 2025Article
- Head and Neck Cancer in Fanconi Anemia: Clinical Challenges and Molecular Insights into a DNA Repair Disorder.Cancers · 2025Review
- Development of translational read-through-inducing drugs as novel therapeutic options for patients with Fanconi anemia.Cell death discovery · 2025Article
- To cleave or not and how? The DNA exonucleases and endonucleases in immunity.Genes & diseases · 2025Review
- Case Report: Eltrombopag in mosaic and gene therapy-treated patients with Fanconi anemia.Frontiers in pediatrics · 2025Article
- LINE-1 hypomethylation characterizes the inflammatory response in coeliac disease associated-intestinal mucosa and small bowel adenocarcinomas.The Journal of pathology · 2025Article
- Contribution of p53-dependent and -independent mechanisms to upregulation of p21 in Fanconi anemia.PLoS genetics · 2024Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fanconi Anemia (FA) is a genetic disorder characterized by elevated cancer susceptibility and pro-inflammatory cytokine production. Using SLX4(FANCP) deficiency as a working model, we questioned the trigger for chronic inflammation in FA. We found that absence of SLX4 caused cytoplasmic DNA accumulation, including sequences deriving from active Long INterspersed Element-1 (LINE-1), triggering the cGAS-STING pathway to elicit interferon (IFN) expression. In agreement, absence of SLX4 leads to upregulated LINE-1 retrotransposition. Importantly, similar results were obtained with the FANCD2 upstream activator of SLX4. Furthermore, treatment of FA cells with the Tenofovir reverse transcriptase inhibitor (RTi), that prevents endogenous retrotransposition, decreased both accumulation of cytoplasmic DNA and pro-inflammatory signaling. Collectively, our data suggest a contribution of endogenous RT activities to the generation of immunogenic cytoplasmic nucleic acids responsible for inflammation in FA. The additional observation that RTi decreased pro-inflammatory cytokine production induced by DNA replication stress-inducing drugs further demonstrates the contribution of endogenous RTs to sustaining chronic inflammation. Altogether, our data open perspectives in the prevention of adverse effects of chronic inflammation in tumorigenesis.
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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.