ArticlePloS one2012
Cdt1 is differentially targeted for degradation by anticancer chemotherapeutic drugs.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
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- Small Molecule Inhibitor Targeting CDT1/Geminin Protein Complex Promotes DNA Damage and Cell Death in Cancer Cells.Frontiers in pharmacology · 2022Article
- SIRT3 promotion reduces resistance to cisplatin in lung cancer by modulating the FOXO3/CDT1 axis.Cancer medicine · 2021Article
- A Custom Ultra-Low-Cost 3D Bioprinter Supports Cell Growth and Differentiation.Frontiers in bioengineering and biotechnology · 2020Article
- CRL4 ubiquitin ligase stimulates Fanconi anemia pathway-induced single-stranded DNA-RPA signaling.BMC cancer · 2019Article
- Prevention of oral carcinogenesis in rats by Dracaena cinnabari resin extracts.Clinical oral investigations · 2019Article
- Direct binding of Cdt2 to PCNA is important for targeting the CRL4Life science alliance · 2018Article
- Mismatch repair proteins recruited to ultraviolet light-damaged sites lead to degradation of licensing factor Cdt1 in the G1 phase.Cell cycle (Georgetown, Tex.) · 2017Article
- Cell cycle staging of individual cells by fluorescence microscopy.Nature protocols · 2015Article
- Mitotic UV irradiation induces a DNA replication-licensing defect that potentiates G1 arrest response.PloS one · 2015Article
- Generation of cell-based systems to visualize chromosome damage and translocations in living cells.Nature protocols · 2014Article
- The stress phenotype makes cancer cells addicted to CDT2, a substrate receptor of the CRL4 ubiquitin ligase.Oncotarget · 2014Article
- PIP degron proteins, substrates of CRL4Cdt2, and not PIP boxes, interfere with DNA polymerase η and κ focus formation on UV damage.Nucleic acids research · 2014Article
- REGγ deficiency promotes premature aging via the casein kinase 1 pathway.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
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Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMaintenance of genome integrity is crucial for the propagation of the genetic information. Cdt1 is a major component of the pre-replicative complex, which controls once per cell cycle DNA replication. Upon DNA damage, Cdt1 is rapidly targeted for degradation. This targeting has been suggested to safeguard genomic integrity and prevent re-replication while DNA repair is in progress. Cdt1 is deregulated in tumor specimens, while its aberrant expression is linked with aneuploidy and promotes tumorigenesis in animal models. The induction of lesions in DNA is a common mechanism by which many cytotoxic anticancer agents operate, leading to cell cycle arrest and apoptosis. METHODOLOGY/PRINCIPAL FINDING: In the present study we examine the ability of several anticancer drugs to target Cdt1 for degradation. We show that treatment of HeLa and HepG2 cells with MMS, Cisplatin and Doxorubicin lead to rapid proteolysis of Cdt1, whereas treatment with 5-Fluorouracil and Tamoxifen leave Cdt1 expression unaffected. Etoposide affects Cdt1 stability in HepG2 cells and not in HeLa cells. RNAi experiments suggest that Cdt1 proteolysis in response to MMS depends on the presence of the sliding clamp PCNA. CONCLUSION/SIGNIFICANCE: Our data suggest that treatment of tumor cells with commonly used chemotherapeutic agents induces differential responses with respect to Cdt1 proteolysis. Information on specific cellular targets in response to distinct anticancer chemotherapeutic drugs in different cancer cell types may contribute to the optimization of the efficacy of chemotherapy.
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