ArticleScience advances2024
Activation of endogenous retroviruses and induction of viral mimicry by MEK1/2 inhibition in pancreatic cancer.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- The therapeutic potential of transposable element activity modulation.EMBO molecular medicine · 2026Review
- SNHG10 promotes tumorigenesis through the EGFR/AKT/ERK/mTOR and miR-150-5p/VEGF-A axis, along with gemcitabine resistance in pancreatic ductal adenocarcinoma.Cell death discovery · 2026Article
- WNT inhibition activates interferon stimulated gene expression by alleviating epigenetic repression of endogenous retroviruses.Scientific reports · 2026Article
- Machine learning-powered single-molecule cancer diagnosis using DNA origami tags.Science advances · 2026Article
- Endogenous retroviruses and response to immune checkpoint inhibitors: mechanisms, clinical evidence, and therapeutic implications.Frontiers in immunology · 2026Review
- Activation of endogenous retroviruses in tumor cells and their immunomodulatory mechanisms: from molecular basis to clinical translation.Frontiers in oncology · 2026Review
- BeyondInternational journal of molecular sciences · 2025Article
- Navigating established and emerging biomarkers for immune checkpoint inhibitor therapy.Cancer cell · 2025Review
- KRASMolecular oncology · 2025Article
- Exploring viral mimicry combined with epigenetics and tumor immunity: new perspectives in cancer therapy.International journal of biological sciences · 2025Review
- Epigenetic control of antigen presentation failure in osteosarcoma: from single-cell chromatin maps to therapeutic strategies.Frontiers in immunology · 2025Review
- Evolution of Repetitive Elements, Their Roles in Homeostasis and Human Disease, and Potential Therapeutic Applications.Biomolecules · 2024Review
- Review
- An integrative epigenome-based strategy for unbiased functional profiling of clinical kinase inhibitors.Molecular systems biology · 2024Article
Corrections and comments
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Authors and funding
23 authors at 4 institutions in 3 countries.
Funding
Abstract
While pancreatic ductal adenocarcinomas (PDACs) are addicted to KRAS-activating mutations, inhibitors of downstream KRAS effectors, such as the MEK1/2 kinase inhibitor trametinib, are devoid of therapeutic effects. However, the extensive rewiring of regulatory circuits driven by the attenuation of the KRAS pathway may induce vulnerabilities of therapeutic relevance. An in-depth molecular analysis of the transcriptional and epigenomic alterations occurring in PDAC cells in the initial hours after MEK1/2 inhibition by trametinib unveiled the induction of endogenous retroviruses (ERVs) escaping epigenetic silencing, leading to the production of double-stranded RNAs and the increased expression of interferon (IFN) genes. We tracked ERV activation to the early induction of the transcription factor ELF3, which extensively bound and activated nonsilenced retroelements and synergized with IRF1 (interferon regulatory factor 1) in the activation of IFNs and IFN-stimulated genes. Trametinib-induced viral mimicry in PDAC may be exploited in the rational design of combination therapies in immuno-oncology.
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Registered trials
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.