The mismatch repair‐mediated cell cycle checkpoint response to fluorodeoxyuridine
Open accessAbstract
The loss of DNA mismatch repair (MMR) is responsible for hereditary nonpolyposis colorectal cancer and a subset of sporadic tumors. Acquired resistance or tolerance to some anti‐cancer drugs occurs when MMR function is impaired. 5‐Fluorouracil (FU), an anti‐cancer drug used in the treatment of advanced colorectal and other cancers, and its metabolites are incorporated into RNA and DNA and inhibit thymidylate synthase resulting in depletion of dTTP and incorporation in DNA of uracil. Although the MMR deficiency has been implicated in tolerance to FU, the mechanism of cell killing remains unclear. Here, we examine the cellular response to fluorodeoxyuridine (FdU) and the role of the MMR system. After brief exposure of cells to low doses of FdU, MMR mediates DNA damage signaling during S‐phase and triggers arrest in G2/M in the first cell cycle in a manner requiring MutSα, MutLα, and DNA replication. Cell cycle arrest is mediated by ATR kinase and results in phosphorylation of Chk1 and SMC1. MutSα binds FdU:G mispairs in vitro consistent with its being a DNA damage sensor. Prolonged treatment with FdU results in an irreversible arrest in G2 that is independent of MMR status and leads to the accumulation of DNA lesions that are targeted by the base excision repair (BER) pathway. Thus, MMR can act as a direct sensor of FdU‐mediated DNA lesions eliciting cell cycle arrest via the ATR/Chk1 pathway. However, at higher levels of damage, other damage surveillance pathways such as BER also play important roles. J. Cell. Biochem. 105: 245–254, 2008. © 2008 Wiley‐Liss, Inc.
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The anticancer drug FdU may generate FdU:G mismatch pairs by being incorporated directly during DNA replication.
“the anticancer drug 5-fluoro-2′-deoxyuridine (FdU), which may cause mismatch pairs of FdU:G via direct incorporation during DNA replication.”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [209]
FdU treatment during S phase activates ATR-Chk1-dependent DDR in a manner requiring MutSα and MutLα.
“ATR-Chk1-dependent DDR is activated by FdU treatment during S phase in a MutSα- and MutLα-dependent manner [209]”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [209]
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- Authors
- Liu, A., Yoshioka, K., Salerno, V., & Hsieh, P.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Hsieh, Peggy
- Venue
- Journal of Cellular Biochemistry
- Publisher
- Wiley
- Published
- 2008-08-21
- Volume
- 105
- Issue
- 1
- Pages
- 245-254
- ISSN
- 0730-2312 (ISSN-L)
- 1097-4644
- PMC
- PMC2562697
- OpenAlex
- W2114105734
- Cited by
- 50
- References
- 39
- Citations by year
- 2026: 1 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 3 · 2018: 1 · 2017: 1 · 2016: 2 · 2015: 4 · 2014: 4 · 2013: 5 · 2012: 4
- FWCI
- 2.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Cellular Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (Z01DK052029)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- DNA mismatch repair, fluorodeoxyuridine, 5-fluorouracil, cell cycle checkpoints, G2/M cell cycle arrest, ATR kinase, Chk1 phosphorylation, SMC1A, MutSα, MutLα, base excision repair, DNA damage signaling, drug tolerance, colorectal cancer, thymidylate synthase inhibition
- MeSH terms
- Checkpoint Kinase 1, Cell Cycle, Enzyme Activation, Floxuridine, Humans, Hydroxylamines, Protein Kinases, Signal Transduction, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Cell Line, Tumor, MutS DNA Mismatch-Binding Protein, DNA Mismatch Repair, Ataxia Telangiectasia Mutated Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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