Combined Haploinsufficiency for ATM and RAD9 as a Factor in Cell Transformation, Apoptosis, and DNA Lesion Repair Dynamics
Open accessAbstract
Loss of function of oncogenes, tumor suppressor genes and DNA damage processing genes has been implicated in the development of many types of cancer, but for the vast majority of cases, there is no link to specific germ line mutations. In the last several years, heterozygosity leading to haploinsufficiency for proteins involved in DNA repair pathways was shown to play a role in genomic instability and carcinogenesis after DNA damage is induced. Because the effect of haploinsufficiency for one protein is relatively small, we hypothesize that predisposition to cancer could be a result of the additive effect of heterozygosity for two or more genes, critical for pathways that control DNA damage signaling, repair or apoptosis. To address this issue, primary mouse cells, haploinsufficient for one or two proteins, ATM and RAD9, related to the cellular response to DNA damage were examined. The results show that cells having low levels of both ATM and RAD9 proteins are more sensitive to transformation by radiation, have different DNA double-strand break repair dynamics and are less apoptotic when compared with wild-type controls or those cells haploinsufficient for only one of these proteins. Our conclusions are that under stress conditions, the efficiency and capacity for DNA repair mediated by the ATM/RAD9 cell signaling network depend on the abundance of both proteins and that, in general, DNA repair network efficiencies are genotype-dependent and can vary within a specific range.
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Haploinsufficiency of checkpoint factors ATM or Rad9 changes double-strand break repair dynamics, implying that checkpoint pathways may control DNA repair quantitatively.
“Strikingly, even haploinsufficiency of checkpoint factors (ATM/Rad9) leads to different double-strand break repair dynamics, implying that checkpoint pathways may control DNA repair activity quantitatively (28).”
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Self-citation
- Authors
- Smilenov, L. B., Lieberman, H. B., Mitchell, S. A., Baker, R. A., Hopkins, K. M., & Hall, E. J.
- Affiliations
- Columbia University (US)
- Rigshospitalet (DK)
- ORCID
- Hall, Eric J.
- Venue
- Cancer Research
- Published
- 2005-02-01
- Volume
- 65
- Issue
- 3
- Pages
- 933-938
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2116106546
- Cited by
- 32
- References
- 38
- Citations by year
- 2023: 1 · 2018: 1 · 2017: 2 · 2014: 2 · 2013: 1 · 2012: 2
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Energy (DE‐FG02‐, FG02-03ER63629)
- National Aeronautics and Space Administration (NAG91519)
- Radiological Society of North America
- National Institutes of Health
- National Cancer Institute (CA 89816, R01CA089816)
- National Institute of General Medical Sciences (R01GM052493, GM 52493)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- haploinsufficiency, ATM, Rad9, DNA double-strand break repair, cell transformation, radiation-induced transformation, apoptosis, DNA damage response, genomic instability, cancer susceptibility, heterozygosity
- MeSH terms
- Animals, Cell Transformation, Neoplastic, DNA Damage, DNA Repair, DNA-Binding Proteins, Female, Haplotypes, Pregnancy, Thymus Gland, Apoptosis, Protein Serine-Threonine Kinases, Mice, Knockout, Cell Cycle Proteins, Tumor Suppressor Proteins, Mice, Ataxia Telangiectasia Mutated Proteins
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