ArticleCell death discovery2025
Activation of APOBEC3 cytidine deaminases and endogenous retroviruses is integrated by MUC1-C in NSCLC cells.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- M1C is a druggable target for NSCLC KRAS G12C mutant tumors resistant to KRAS inhibitors.Oncogene · 2026Article
- Evolution ofInternational journal of molecular sciences · 2026Review
- Evolution of the MUC1 gene in eutherian mammals as an adaptation responsible for the increasing incidence of cancer in humans.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Plasma HERV-K envelopE RNA: a minimally invasive biomarker for lung adenocarcinoma detection and prognostic assessment in the context of conventional serum tumor markers.Frontiers in immunology · 2026Article
- Host genetic determinants of resistance and susceptibility to bovine leukemia virus infection: A mini-review.Molecular biology reports · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
The APOBEC3 (A3) genes encoding cytidine deaminases evolved in mammals to restrict retroviral replication. The MUC1 gene appeared in mammals to protect barrier tissues from viral infections. There is no known involvement of the MUC1 encoded MUC1-C/M1C protein in the regulation of A3s. We found that induction of MUC1-C in NSCLC cells treated with EGFR inhibitors integrates activation of an inflammatory memory response with the type I interferon (IFN) STAT1/STAT2/IRF9 (U-ISGF3) pathway. In turn, MUC1-C drives expression of A3 genes by activating their U-ISGF3-stimulated response elements (ISREs). We also report that MUC1-C-mediated induction of type II IFN STAT1 homodimer (U-GAF) complexes and the gamma-associated signaling (GAS) pathway drives human endogenous retrovirus HERV-K102/K108 expression. Our results in NSCLC cell line and patient-derived models further demonstrate that MUC1-C activates A3 and HERV-K expression by a common MUC1-C→STAT1 auto-inductive pathway. These previously unrecognized findings demonstrate that a MUC1-C-driven inflammatory pathway coordinates activation of APOBEC3 and HERV-K expression.
Identifiers
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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.