ReviewAnti-cancer agents in medicinal chemistry2008
In vivo roles of CDC25 phosphatases: biological insight into the anti-cancer therapeutic targets.
Review in Anti-cancer agents in medicinal chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 77 citations in OpenAlex.
- Novel CDK-independent function of CDC25 phosphatases in mRNA translation.EMBO reports · 2026Article
- Mitotic Disruption and Cytoskeletal Alterations Induced byInternational journal of molecular sciences · 2025Article
- The phosphatase CTDSPL2 promotes proliferation, invasion, metastasis and regorafenib resistance in osteosarcoma.Journal of bone oncology · 2025Article
- Sulforaphane-Induced Cell Mitotic Delay and Inhibited Cell Proliferation via Regulating CDK5R1 Upregulation in Breast Cancer Cell Lines.Biomedicines · 2023Article
- Semisynthetic aurones A14 protects against T-cell acute lymphoblastic leukemia via suppressing proliferation and inducing cell cycle arrest with apoptosis.Chinese medicine · 2022Article
- The phosphatase CTDSPL2 is phosphorylated in mitosis and a target for restraining tumor growth and motility in pancreatic cancer.Cancer letters · 2022Article
- Article
- JNK-dependent cell cycle stalling in G2 promotes survival and senescence-like phenotypes in tissue stress.eLife · 2019Article
- Therapeutic efficacy of a novel βIII/βIV-tubulin inhibitor (VERU-111) in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2019Article
- Identification of tumor antigens in malignant mesothelioma.Oncology letters · 2017Article
- Proteomics insights into DNA damage response and translating this knowledge to clinical strategies.Proteomics · 2017Review
- Induction of Mitotic Delay in Pharyngeal and Nasopharyngeal Carcinoma Cells Using an Aqueous Extract ofInternational journal of medical sciences · 2017Article
- Phosphorylation of CDC25A on SER283 in late S/G2 by CDK/cyclin complexes accelerates mitotic entry.Cell cycle (Georgetown, Tex.) · 2016Article
- Coexistence of YWHAZ amplification predicts better prognosis in muscle-invasive bladder cancer with CDKN2A or TP53 loss.Oncotarget · 2016Article
- Article
- Novel 3-Substituted 7-Phenylpyrrolo[3,2-f]quinolin-9(6H)-ones as Single Entities with Multitarget Antiproliferative Activity.Journal of medicinal chemistry · 2015Article
- Design, synthesis, in vitro, and in vivo anticancer and antiangiogenic activity of novel 3-arylaminobenzofuran derivatives targeting the colchicine site on tubulin.Journal of medicinal chemistry · 2015Article
- MHC-restricted phosphopeptides from insulin receptor substrate-2 and CDC25b offer broad-based immunotherapeutic agents for cancer.Cancer research · 2014Article
- A PREVIOUSLY UNKNOWN UNIQUE CHALLENGE FOR INHIBITORS OF SYK ATP-BINDING SITE: ROLE OF SYK AS A CELL CYCLE CHECKPOINT REGULATOR.EBioMedicine · 2014Article
- Design, synthesis and biological evaluation of 3,5-disubstituted 2-amino thiophene derivatives as a novel class of antitumor agents.Bioorganic & medicinal chemistry · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
CDC25 phosphatases are not only rate-limiting activators of cyclin-dependent kinases (CDKs) but also important targets of the CHK1/CHK2-mediated checkpoint pathway. Each isoform of the mammalian CDC25 family seems to exert unique biological functions. CDC25A is a critical regulator for both G1-S and G2-M transitions and essential for embryonic cell proliferation after the blastocyst stage. CDC25B is dispensable for embryogenesis but required for meiotic progression of oocytes in a manner analogous to Drosophila Twine or C. elegans cdc-25.1. Moreover, CDC25A and CDC25B appear to regulate different events or stages of mitosis. CDC25B may mediate the activation of CDK1/Cyclin B at the centrosome during prophase, while CDC25A may be required for the subsequent full activation of nuclear CDK1/Cyclin B. CDC25C is dispensable for both mitotic and meiotic divisions, although it is highly regulated during the processes. Excessive levels of CDC25A and CDC25B are often observed in various human cancer tissues. Deregulated expression of these phosphatases allows cells to overcome DNA damage-induced checkpoint, leading to genomic instability. Studies using mouse models demonstrated that deregulated expression of CDC25A significantly promotes RAS- or NEU-induced mammary tumor development with chromosomal aberrations, whereas decreased CDC25A expression in heterozygous knockout mice delays tumorigenesis. These biological properties of CDC25 phosphatases provide significant insight into the pathobiology of cancer and scientific foundation for anti-CDC25 therapeutic intervention.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.