Nuclear Receptor-Induced Chromosomal Proximity and DNA Breaks Underlie Specific Translocations in Cancer
Open accessAbstract
Chromosomal translocations are a hallmark of leukemia/lymphoma and also appear in solid tumors, but the underlying mechanism remains elusive. By establishing a cellular model that mimics the relative frequency of authentic translocation events without proliferation selection, we report mechanisms of nuclear receptor-dependent tumor translocations. Intronic binding of liganded androgen receptor (AR) first juxtaposes translocation loci by triggering intra- and interchromosomal interactions. AR then promotes site-specific DNA double-stranded breaks (DSBs) at translocation loci by recruiting two types of enzymatic activities induced by genotoxic stress and liganded AR, including activation-induced cytidine deaminase and the LINE-1 repeat-encoded ORF2 endonuclease. These enzymes synergistically generate site-selective DSBs at juxtaposed translocation loci that are ligated by nonhomologous end joining pathway for specific translocations. Our data suggest that the confluence of two parallel pathways initiated by liganded nuclear receptor and genotoxic stress underlies nonrandom tumor translocations, which may function in many types of tumors and pathological processes.
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NHEJ is error-prone and can cause genome structural variations, potentially leading to gene fusions with pathological gain or loss of function.
“NEHJ is error-prone and can cause genome structural variations, potentially leading to gene fusions with pathological gain or loss of function”
From Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration (2023) · cites this paper as [20]
DSBs are repaired via the classical non-homologous end joining (NHEJ) pathway in post-mitotic cells and can lead to genome structural variations.
“DSBs are repaired via the classical non-homologous end joining (NHEJ) pathway in post-mitotic cells and can lead to genome structural variations”
From Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration (2023) · cites this paper as [20]
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- Authors
- Lin, C., Yang, L., Tanasa, B., Hutt, K., Ju, B.-G., Ohgi, K. A., Zhang, J., Rose, D. W., Fu, X.-D., Glass, C. K., & Rosenfeld, M. G.
- Affiliations
- Howard Hughes Medical Institute (US)
- University of California San Diego (US)
- Corresponding author
- Rosenfeld, Michael G.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 139
- Issue
- 6
- Pages
- 1069-1083
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC2812435
- OpenAlex
- W2104400024
- Cited by
- 576
- References
- 59
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 5 · 2023: 18 · 2022: 17 · 2021: 27 · 2020: 15 · 2019: 23 · 2018: 29 · 2017: 38 · 2016: 36 · 2015: 38 · 2014: 58 · 2013: 81 · 2012: 52
- FWCI
- 23.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- Prostate Cancer Foundation
- Susan G. Komen
- National Institutes of Health
- U.S. Public Health Service (KG080247)
- National Heart, Lung, and Blood Institute (R01HL065445)
- National Cancer Institute (R01CA097134, CA97134)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK39949, DK-18477, R37DK039949, R01DK018477)
- National Institute of Neurological Disorders and Stroke (R01NS034934, NS 34934)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- chromosomal translocation, nuclear receptors, androgen receptor, DNA double-strand breaks, activation-induced cytidine deaminase, non-homologous end joining, genotoxic stress, interchromosomal interactions, leukemia, solid tumors
- MeSH terms
- Transcriptional Regulator ERG, DNA Damage, DNA Repair, DNA-Binding Proteins, Humans, Introns, Male, Prostatic Neoplasms, Receptors, Androgen, Serine Endopeptidases, Transcription Factors, Transcription, Genetic, Translocation, Genetic, Trans-Activators, Open Reading Frames, Long Interspersed Nucleotide Elements, Cell Line, Tumor
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