The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Loss of the Forkhead Transcription Factor FoxM1 Causes Centrosome Amplification and Mitotic Catastrophe
Open accessAbstract
Expression of the forkhead transcription factor FoxM1 correlates with proliferative status in a variety of normal and transformed cell types. Elevated expression of FoxM1 has been noted in both hepatocellular carcinoma and basal cell carcinoma. However, whether FoxM1 expression is essential for the viability of transformed cells is unknown. We report here that the expression of FoxM1 is significantly elevated in primary breast cancer. Microarray analysis shows that FoxM1 regulates genes that are essential for faithful chromosome segregation and mitosis, including Nek2, KIF20A, and CENP-A. Loss of FoxM1 expression generates mitotic spindle defects, delays cells in mitosis, and induces mitotic catastrophe. Time-lapse microscopy indicates that depletion of FoxM1 generates cells that enter mitosis but are unable to complete cell division, resulting in either mitotic catastrophe or endoreduplication. These findings indicate that FoxM1 depletion causes cell death due to mitotic catastrophe and that inhibiting FoxM1 represents a therapeutic strategy to target breast cancer.
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Self-citationCdi1, a human G1 and S phase protein phosphatase that associates with Cdk2
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Cited by
The emerging roles of forkhead box (Fox) proteins in cancer
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Basal cell carcinomas: attack of the hedgehog
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Death through a tragedy: mitotic catastrophe
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Metadata
- Authors
- Wonsey, D. R., & Follettie, M. T.
- Venue
- Cancer Research
- Published
- 2005-06-15
- Volume
- 65
- Issue
- 12
- Pages
- 5181-5189
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2034091087
- Cited by
- 349
- References
- 45
- FWCI
- 6.55
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Wonsey, D. R., & Follettie, M. T. (2005). Loss of the Forkhead Transcription Factor FoxM1 Causes Centrosome Amplification and Mitotic Catastrophe. Cancer Research. https://doi.org/10.1158/0008-5472.can-04-4059
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
