The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Cyclin D1 Is Required for Transformation by Activated Neu and Is Induced through an E2F-Dependent Signaling Pathway
Open accessAbstract
The neu (c-erbB-2) proto-oncogene encodes a tyrosine kinase receptor that is overexpressed in 20 to 30% of human breast tumors. Herein, cyclin D1 protein levels were increased in mammary tumors induced by overexpression of wild-type Neu or activating mutants of Neu in transgenic mice and in MCF7 cells overexpressing transforming Neu. Analyses of 12 Neu mutants in MCF7 cells indicated important roles for specific C-terminal autophosphorylation sites and the extracellular domain in cyclin D1 promoter activation. Induction of cyclin D1 by NeuT involved Ras, Rac, Rho, extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38, but not phosphatidylinositol 3-kinase. NeuT induction of the cyclin D1 promoter required the E2F and Sp1 DNA binding sites and was inhibited by dominant negative E2F-1 or DP-1. Neu-induced transformation was inhibited by a cyclin D1 antisense or dominant negative E2F-1 construct in Rat-1 cells. Growth of NeuT-transformed mammary adenocarcinoma cells in nude mice was blocked by the cyclin D1 antisense construct. These results demonstrate that E2F-1 mediates a Neu-signaling cascade to cyclin D1 and identify cyclin D1 as a critical downstream target of neu-induced transformation.
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Cited by
Cyclin D as a therapeutic target in cancer
Musgrove, E. A., Caldon, C. E., Barraclough, J., Stone, A., & Sutherland, R. L. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3090 · Cited by 1,370
Treating cancer with selective CDK4/6 inhibitors
O'Leary, B., Finn, R. S., & Turner, N. C. (2016) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2016.26 · Cited by 1,137
Sp1 and krüppel‐like factor family of transcription factors in cell growth regulation and cancer
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Specific protection against breast cancers by cyclin D1 ablation
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Cyclin D1, cancer progression, and opportunities in cancer treatment
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Metadata
- Authors
- Lee, R. J., Albanese, C., Fu, M., D'Amico, M., Lin, B., Watanabe, G., Haines, G. K., Siegel, P. M., Hung, M.-C., Yarden, Y., Horowitz, J. M., Muller, W. J., & Pestell, R. G.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2000-01-15
- Volume
- 20
- Issue
- 2
- Pages
- 672-683
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- OpenAlex
- W2147746178
- Cited by
- 347
- References
- 5
- FWCI
- 13.50
- Type
- journal article
- Language
- en
- Open access
- green
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- Lee, R. J., Albanese, C., Fu, M., D'Amico, M., Lin, B., Watanabe, G., Haines, G. K., Siegel, P. M., Hung, M.-C., Yarden, Y., Horowitz, J. M., Muller, W. J., & Pestell, R. G. (2000). Cyclin D1 Is Required for Transformation by Activated Neu and Is Induced through an E2F-Dependent Signaling Pathway. Molecular and Cellular Biology. https://doi.org/10.1128/mcb.20.2.672-683.2000
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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.
