Cited by 175Telomeres, Telomerase, and SenescenceBiochemical and Molecular ResearchDNA Repair Mechanisms

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Nucleotide metabolism, oncogene-induced senescence and cancer

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Aird, Katherine M., Zhang, Rugang·2015·Cancer Letters

DOI 10.1016/j.canlet.2014.01.017PMC PMC4115046

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Abstract

Senescence is defined as a stable cell growth arrest. Oncogene-induced senescence (OIS) occurs when an activated oncogene is expressed in a normal cell. OIS acts as a bona fide tumor suppressor mechanism by driving stable growth arrest of cancer progenitor cells harboring the initial oncogenic hit. OIS is often characterized by aberrant DNA replication and the associated DNA damage response. Nucleotides, in particular deoxyribonucleotide triphosphates (dNTPs), are necessary for both DNA replication and repair. Imbalanced dNTP pools play a role in a number of human diseases, including during the early stages of cancer development. This review will highlight what is currently known about the role of decreased nucleotide metabolism in OIS, how nucleotide metabolism leads to transformation and tumor progression, and how this pathway can be targeted as a cancer therapeutic by inducing senescence of cancer cells.

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Additional file 9 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
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Additional file 3 of MYBL2 regulates de novo purine synthesis by transcriptionally activating IMPDH1 in hepatocellular carcinoma cells
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Additional file 5 of MYBL2 regulates de novo purine synthesis by transcriptionally activating IMPDH1 in hepatocellular carcinoma cells
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Additional file 2 of MYBL2 regulates de novo purine synthesis by transcriptionally activating IMPDH1 in hepatocellular carcinoma cells
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Additional file 18 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
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Additional file 8 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
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Additional file 14 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
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Additional file 11 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
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Additional file 5 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
Liu, J., Li, H., Wang, L., Wang, S., & Tang, Q. (2024) · Figshare · doi:10.6084/m9.figshare.26755552
Additional file 15 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
Liu, J., Li, H., Wang, L., Wang, S., & Tang, Q. (2024) · Figshare · doi:10.6084/m9.figshare.26755582
Additional file 2 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
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Additional file 6 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
Liu, J., Li, H., Wang, L., Wang, S., & Tang, Q. (2024) · Figshare · doi:10.6084/m9.figshare.26755555
Additional file 4 of MYBL2 regulates de novo purine synthesis by transcriptionally activating IMPDH1 in hepatocellular carcinoma cells
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Additional file 12 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
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Additional file 1 of MYBL2 regulates de novo purine synthesis by transcriptionally activating IMPDH1 in hepatocellular carcinoma cells
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Additional file 7 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
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Additional file 19 of Spatial transcriptome and single-cell reveal the role of nucleotide metabolism in colorectal cancer progression and tumor microenvironment
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Authors: Aird, K. M., & Zhang, R.
Affiliations: The Wistar Institute (US)
Corresponding author: Zhang, Rugang
ORCID: Aird, Katherine M.
Zhang, Rugang
Venue: Cancer Letters
Publisher: Elsevier BV
Published: 2015-01
Volume: 356
Issue: 2
Pages: 204-210
ISSN: 0304-3835 (ISSN-L)
DOI: 10.1016/j.canlet.2014.01.017
PMC: PMC4115046
OpenAlex: W1974913955
Cited by: 166
References: 109
Citations by year: 2026: 9 · 2025: 10 · 2024: 31 · 2023: 17 · 2022: 22 · 2021: 17 · 2020: 11 · 2019: 10 · 2018: 11 · 2017: 6 · 2016: 12 · 2015: 6
FWCI: 1.10
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Cancer Letters (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (CA010815, T32CA9171-35, R01CA160331, R01CA163377, T32CA009171, P30CA010815)
Ovarian Cancer Academy
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Biochemical and Molecular Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Keywords: oncogene-induced senescence, nucleotide metabolism, dNTP pools, DNA replication, DNA damage response, tumor suppression, tumor progression, cellular senescence, cancer therapy, DNA repair
MeSH terms: Cell Transformation, Neoplastic, Deoxyribonucleotides, DNA Damage, DNA Repair, DNA Replication, Humans, Neoplasms, Oncogenes, Biomarkers, Tumor, Neoplastic Stem Cells, Signal Transduction, Cellular Senescence, Cell Proliferation

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Nucleotide metabolism, oncogene-induced senescence and cancer

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