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Cited by 657

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 access
Qie, Shuo, Diehl, J. Alan·2016·Journal of Molecular Medicine

Abstract

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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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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CoChat. (2026). Citation check: Cyclin D1, cancer progression, and opportunities in cancer treatment. https://app.cochat.ai/papers/10.1007/s00109-016-1475-3
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Qie, S., & Diehl, J. A. (2016). Cyclin D1, cancer progression, and opportunities in cancer treatment. Journal of Molecular Medicine. https://doi.org/10.1007/s00109-016-1475-3

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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.