Vitamin D/vitamin D receptor axis regulates DNA repair during oncogene-induced senescence
Open accessAbstract
Oncogenic Ras expression is associated with activation of the DNA damage response (DDR) pathway, as evidenced by elevated DNA damage, primarily DNA double-strand breaks (DSBs), and activation of DNA damage checkpoints, which in primary human cells leads to entry into senescence. DDR activation is viewed as a physiological barrier against uncontrolled proliferation in oncogenic Ras-expressing cells, and arises in response to genotoxic stress due to the production of reactive oxygen species that damage DNA and to hyper-replication stress. Although oncogene-induced senescence (OIS) is considered a tumor suppressor mechanism, the accumulation of DNA damage in senescent cells is thought to cause genomic instability, eventually allowing secondary hits in the genome that promote tumorigenesis. To date, the molecular mechanisms behind DNA repair defects during OIS remain poorly understood. Here, we show that oncogenic Ras expression in human primary cells results in the downregulation of BRCA1 and 53BP1, two key factors in DNA DSB repair by homologous recombination and non-homologous end joining, respectively. As a consequence, Ras-induced senescent cells are hindered in their ability to recruit BRCA1 and 53BP1 to DNA damage sites. Whereas BRCA1 is downregulated at transcripts levels, 53BP1 loss is caused by activation of cathepsin L-mediated degradation of 53BP1 protein. Moreover, we discovered a marked downregulation of vitamin D receptor (VDR) during OIS, and a role for the vitamin D/VDR axis regulating the levels of these DNA repair factors during OIS. This study reveals a new functional relationship between the oncogene Ras, the vitamin D/VDR axis and the expression of DNA repair factors, in the context of OIS. The observed deficiencies in DNA repair factors in senescent cells could contribute to the genomic instability that allows senescence bypass and tumorigenesis.
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The mechanism by which DNA repair genes are down-regulated in association with cellular senescence may be due to chronically increased levels of oxidative stress associated with a pro-inflammatory toxic environment.
“The mechanism by which DNA repair genes are down-regulated in association with cellular senescence, is not entirely clear, but may be due to chronically increased levels of oxidative stress associated with a pro-inflammatory toxic environment [49].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [49]
Transcriptional repression of DNA repair genes is a hallmark of senescence.
“Consistent with studies showing that transcriptional repression of DNA repair genes is a hallmark of senescence [49]”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [49]
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Transcriptional repression of DNA repair genes is a hallmark and a cause of cellular senescence
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- Authors
- Graziano, S., Johnston, R., Deng, O., Zhang, J., & Gonzalo, S.
- Affiliations
- Saint Louis University (US)
- Case Western Reserve University (US)
- Corresponding author
- Gonzalo, S
- Venue
- Oncogene
- Published
- 2016-04-04
- Volume
- 35
- Issue
- 41
- Pages
- 5362-5376
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- PMC
- PMC5050051
- OpenAlex
- W2337307831
- Cited by
- 60
- References
- 63
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 2 · 2023: 10 · 2022: 3 · 2021: 5 · 2020: 9 · 2019: 9 · 2018: 8 · 2017: 1 · 2016: 2
- FWCI
- 5.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA154625)
- National Institute of General Medical Sciences (R01GM094513)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Vitamin D Research Studies
- Keywords
- vitamin D, vitamin D receptor, oncogene-induced senescence, DNA repair, DNA double-strand breaks, BRCA1, 53BP1, cathepsin L, Ras, homologous recombination, non-homologous end joining, genomic instability, senescence bypass, carcinogenesis, DNA damage response
- MeSH terms
- Tumor Suppressor p53-Binding Protein 1, Breast Neoplasms, DNA Damage, DNA Repair, Humans, Genes, ras, Vitamin D, Gene Expression Regulation, Neoplastic, Cellular Senescence, Receptors, Calcitriol, BRCA1 Protein, Genomic Instability, DNA Breaks, Double-Stranded, Cathepsin L, Homologous Recombination, MCF-7 Cells, Carcinogenesis
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