The DOI matches its Crossref record; 139 of the 139 references it cites were found in a registry or an index.
Cyclin D1, cancer progression, and opportunities in cancer treatment
Open accessAbstract
Mammalian cells encode three D cyclins (D1, D2, and D3) that coordinately function as allosteric regulators of cyclin-dependent kinase 4 (CDK4) and CDK6 to regulate cell cycle transition from G1 to S phase. Cyclin expression, accumulation, and degradation, as well as assembly and activation of CDK4/CDK6 are governed by growth factor stimulation. Cyclin D1 is more frequently dysregulated than cyclin D2 or D3 in human cancers, and as such, it has been more extensively characterized. Overexpression of cyclin D1 results in dysregulated CDK activity, rapid cell growth under conditions of restricted mitogenic signaling, bypass of key cellular checkpoints, and ultimately, neoplastic growth. This review discusses cyclin D1 transcriptional, translational, and post-translational regulations and its biological function with a particular focus on the mechanisms that result in its dysregulation in human cancers.
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Cites
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The double dealing of cyclin D1
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Wang, B., Peng, F., Huang, W., Zhou, J., Zhang, N., Sheng, J., Haruehanroengra, P., He, G., & Han, B. (2020) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2019.12.013 · Cited by 73
Choi, K. H., Shin, C. H., Lee, W. J., Ji, H., & Kim, H. H. (2019) · Bioscience Reports · doi:10.1042/bsr20190634 · Cited by 42
Nasser, F., Moussa, N., Helmy, M. W., & Haroun, M. (2021) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-020-01988-x · Cited by 29
Metadata
- Authors
- Qie, S., & Diehl, J. A.
- Venue
- Journal of Molecular Medicine
- Published
- 2016-10-02
- Volume
- 94
- Issue
- 12
- Pages
- 1313-1326
- ISSN
- 0946-2716 (ISSN-L)
- 1432-1440
- OpenAlex
- W2527438532
- Cited by
- 657
- References
- 139
- FWCI
- 19.16
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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