ArticleMolecular oncology2018
Epigenetic reactivation of LINE-1 retrotransposon disrupts NuRD corepressor functions and induces oncogenic transformation in human bronchial epithelial cells.
Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: An update of a systematic literature review.Mutation research. Reviews in mutation researchPooled it
- LINE-1 retrotransposons: Multifaceted functions and regulatory mechanisms in health and disease.Molecular therapy. Nucleic acids · 2026Review
- LINE1 insertion into the NACC2 locus disrupts the HDM2 axis and activates lung oncogenic signaling.NPJ precision oncology · 2025Article
- Human cytomegalovirus infection induces L1 expression through UL38-dependent mTOR-KAP1 pathway.PloS one · 2025Article
- The role of cellular senescence in skin aging and age-related skin pathologies.Frontiers in physiology · 2023Review
- Recent progress in targeted therapy for non-small cell lung cancer.Frontiers in pharmacology · 2023Review
- Role of Transposable Elements in Genome Stability: Implications for Health and Disease.International journal of molecular sciences · 2022Review
- Role of long interspersed nuclear element-1 in the regulation of chromatin landscapes and genome dynamics.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Review
- Computational modeling of RNase, antisense ORF0 RNA, and intracellular compartmentation and their impact on the life cycle of the line retrotransposon.Computational and structural biotechnology journal · 2021Article
- Serum levels of L1-ORF1p and airflow limitation.ERJ open research · 2019Article
- Precision prevention: A focused response to shifting paradigms in healthcare.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Long interspersed nuclear element-1 (LINE-1 or L1) reactivation is linked to poor prognosis in non-small-cell lung carcinoma (NSCLC), but the molecular bases of this response remain largely unknown. In this report, we show that challenge of human bronchial epithelial cells (HBECs) with the lung carcinogen, benzo(a)pyrene (BaP), shifted the L1 promoter from a heterochromatic to euchromatic state through disassembly of the nucleosomal and remodeling deacetylase (NuRD) complex. Carcinogen challenge was also associated with partial displacement of constituent proteins from the nuclear to the cytoplasmic compartment. Disruption of NuRD corepression by genetic ablation or carcinogen treatment correlated with accumulation of L1 mRNA and proteins. Mi2β bound directly to the L1 promoter to effect retroelement silencing, and this response required the DNA- and ATPase-binding domains of Mi2β. Sustained expression of L1 in HBECs was tumorigenic in a human-SCID mouse xenograft model, giving rise to tumors that regressed over time. Together, these results show that functional modulation of the NuRD constituent proteins is a critical molecular event in the activation of L1 retrotransposon. L1 expression creates a microenvironment in HBECs that is conducive to neoplasia and malignant transformation.
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