ReviewMolecules (Basel, Switzerland)2014
Therapeutic targeting the cell division cycle 25 (CDC25) phosphatases in human acute myeloid leukemia--the possibility to target several kinases through inhibition of the various CDC25 isoforms.
Review in Molecules (Basel, Switzerland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 82 citations in OpenAlex.
- Multicomponent reactions for protein tyrosine phosphatase inhibitors.Molecular diversity · 2026Review
- The Binding of 3-O-Methylfluorescein Phosphate to the Catalytic Domain of the Human CDC25B Phosphatase: A Structural Investigation.Chembiochem : a European journal of chemical biology · 2026Article
- E2F1 Facilitates the Proliferation and Stemness of Gastric Cancer Cells by Activating CDC25B Transcription and Modulating the MAPK Pathway.Biochemical genetics · 2025Article
- Circadian Gene NPAS2 Relieves Hypertrophic Scar Formation via CDC25A-Mediated Fibroblasts Activity.Journal of cellular and molecular medicine · 2025Article
- BKT300: A Novel Anti-Leukemic Small Molecule Targeting the Protein Regulator of Cytokinesis 1 (PRC1) Pathway.Research square · 2025Article
- Cryo-EM structure of the CDK2-cyclin A-CDC25A complex.Nature communications · 2024Article
- Potential of CDC25 phosphatases in cancer research and treatment: key to precision medicine.Frontiers in pharmacology · 2024Review
- The BET inhibitor sensitivity is associated with the expression level of CDC25B in pancreatic cancer models.Cancer drug resistance (Alhambra, Calif.) · 2024Article
- A novel selenium analog of HDACi-based twin drug induces apoptosis and cell cycle arrest via CDC25A to improve prostate cancer therapy.Theranostics · 2024Article
- The Emerging Role of Protein Phosphatase in Regeneration.Life (Basel, Switzerland) · 2023Review
- CDC25A inhibition suppresses cell proliferation and induces GMolecular medicine reports · 2023Article
- Repurposing a Cyclin-Dependent Kinase 1 (CDK1) Mitotic Regulatory Network to Complete Terminal Differentiation in Lens Fiber Cells.Investigative ophthalmology & visual science · 2023Article
- A novel CDC25A/DYRK2 regulatory switch modulates cell cycle and survival.Cell death and differentiation · 2022Article
- Article
- In Silico Identification of Small Molecules as New Cdc25 Inhibitors through the Correlation between Chemosensitivity and Protein Expression Pattern.International journal of molecular sciences · 2021Article
- Bioinformatic analysis linking genomic defects to chemosensitivity and mechanism of action.PloS one · 2021Article
- Inhibition mechanism of naphthylphenylamine derivatives acting on the CDC25B dual phosphatase and analysis of the molecular processes involved in the high cytotoxicity exerted by one selected derivative in melanoma cells.Journal of enzyme inhibition and medicinal chemistry · 2020Article
- Overexpression of Cyclin E1 or Cdc25A leads to replication stress, mitotic aberrancies, and increased sensitivity to replication checkpoint inhibitors.Oncogenesis · 2020Article
- ALOX12B promotes carcinogenesis in cervical cancer by regulating the PI3K/ERK1 signaling pathway.Oncology letters · 2020Article
- B7-H3 promotes the cell cycle-mediated chemoresistance of colorectal cancer cells by regulating CDC25A.Journal of Cancer · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cell division cycle 25 (CDC25) phosphatases include CDC25A, CDC25B and CDC25C. These three molecules are important regulators of several steps in the cell cycle, including the activation of various cyclin-dependent kinases (CDKs). CDC25s seem to have a role in the development of several human malignancies, including acute myeloid leukemia (AML); and CDC25 inhibition is therefore considered as a possible anticancer strategy. Firstly, upregulation of CDC25A can enhance cell proliferation and the expression seems to be controlled through PI3K-Akt-mTOR signaling, a pathway possibly mediating chemoresistance in human AML. Loss of CDC25A is also important for the cell cycle arrest caused by differentiation induction of malignant hematopoietic cells. Secondly, high CDC25B expression is associated with resistance against the antiproliferative effect of PI3K-Akt-mTOR inhibitors in primary human AML cells, and inhibition of this isoform seems to reduce AML cell line proliferation through effects on NFκB and p300. Finally, CDC25C seems important for the phenotype of AML cells at least for a subset of patients. Many of the identified CDC25 inhibitors show cross-reactivity among the three CDC25 isoforms. Thus, by using such cross-reactive inhibitors it may become possible to inhibit several molecular events in the regulation of cell cycle progression and even cytoplasmic signaling, including activation of several CDKs, through the use of a single drug. Such combined strategies will probably be an advantage in human cancer treatment.
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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 Socratic graph.