Differential role of RB in response to UV and IR damage
Open accessAbstract
The retinoblastoma tumor suppressor (RB) is functionally inactivated in the majority of cancers and is a critical mediator of DNA damage checkpoints. Despite the critical importance of RB function in tumor suppression, the coordinate impact of RB loss on the response to environmental and therapeutic sources of damage has remained largely unexplored. Here, we utilized a conditional knockout system to ablate RB in adult fibroblasts. This model system enabled us to investigate the temporal role of RB loss on cell cycle checkpoints and DNA damage repair following ultraviolet (UV) and ionizing radiation (IR) damage. We demonstrate that RB loss compromises rapid cell cycle arrest following UV and IR exposure in adult primary cells. Detailed kinetic analysis of the checkpoint response revealed that disruption of the checkpoint is concomitant with RB target gene deregulation, and is not simply a manifestation of chronic RB loss. RB loss had a differential effect upon repair of the major DNA lesions induced by IR and UV. Whereas RB did not affect resolution of DNA double-strand breaks, RB-deficient cells exhibited accelerated repair of pyrimidine pyrimidone photoproducts (6-4 PP). In parallel, this repair was coupled with enhanced expression of specific factors and the behavior of proliferating cell nuclear antigen (PCNA) recruitment to replication and repair foci. Thus, RB loss and target gene deregulation hastens the repair of specific lesions distinct from its ubiquitous role in checkpoint abrogation.
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In Rb-deficient cells, UV-induced lesions fail to induce cell cycle arrest, but DNA repair mechanisms are rapidly engaged.
“In Rb-deficient cells, UV-induced lesions fail to induce cell cycle arrest, unlike in Rb wild-type cells; however, DNA repair mechanisms are rapidly engaged81.”
From Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008) · cites this paper as [81]
RB has a separate function in the ATR pathway, which responds to single-stranded DNA from stalled replication forks and induces DNA repair.
“RB seems to have a separate function in the ATR (ATM and RAD3-related) pathway, which responds to single-stranded DNA resulting from stalled replication forks and induces DNA repair.”
From Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008) · cites this paper as [81]
Loss of RB may increase apoptotic and autophagic cell death and DNA lesion repair.
“But, loss of RB might also increase apoptotic and autophagic cell death and the ability to repair DNA lesions81,84, which might not be beneficial to tumour cells.”
From Cellular mechanisms of tumour suppression by the retinoblastoma gene (2008) · cites this paper as [81]
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- Authors
- Bosco, E. E.
- Affiliations
- University of Cincinnati (US)
- Corresponding author
- Bosco, E. E.
- ORCID
- Bosco, E. E.
- Venue
- Nucleic Acids Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-03-08
- Volume
- 33
- Issue
- 5
- Pages
- 1581-1592
- ISSN
- 0305-1048 (ISSN-L)
- 1362-4962
- PMC
- PMC1065251
- OpenAlex
- W2052902651
- Cited by
- 24
- References
- 62
- Citations by year
- 2024: 1 · 2022: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2015: 1 · 2014: 1 · 2013: 1 · 2012: 1
- FWCI
- 1.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nucleic Acids Research (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense
- Albert J. Ryan Foundation
- National Institutes of Health
- National Cancer Institute (CA106412)
- National Institute of Environmental Health Sciences (E30-ES 06096, P30ES006096)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- retinoblastoma protein, Rb loss, DNA damage checkpoint, UV damage, ionizing radiation, DNA repair, cell cycle arrest, DNA double-strand break repair
- MeSH terms
- Animals, Cell Cycle, Cells, Cultured, DNA Damage, DNA Repair, Gene Expression Regulation, Kinetics, Radiation, Ionizing, Ultraviolet Rays, Down-Regulation, Retinoblastoma Protein, Mice
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