Suppression of Neu-induced mammary tumor growth in cyclin D1 deficient mice is compensated for by cyclin E
Abstract
Amplification and/or overexpression of the receptor tyrosine kinase HER2/Neu and the cell cycle regulatory gene cyclin D1 are frequently associated with human breast cancer. We studied the functional significance of cyclin D1 in Neu-induced mammary oncogenesis by developing mice overexpressing either wild-type or mutant Neu in a cyclin D1 deficient background. The absence of cyclin D1 suppresses mammary tumor formation induced by the wild-type or activated mutant form of Neu, which promote multi- and single-step progression of tumorigenesis, respectively. These data indicate that cyclin D1 is preferentially required for Neu-mediated signal transduction pathways in mammary oncogenesis. Significantly, 35% of mutant Neu/cyclin D1(-/-) mice regained mammary tumor potential due to compensation by cyclin E. Thus, shared targets of cyclins D1 and E are important in modulating Neu function in mammary tumorigenesis. Our results imply that the combinatorial inhibition of cyclins D1 and E might be useful in the treatment of malignancies induced by Neu.
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Cyclin E can compensate for loss of cyclin D1.
“Furthermore, not only other D type cyclins, but also cyclin E can compensate for loss of D1. 19”
From Interleukin 6 Is Important for Survival After Partial Hepatectomy in Mice (2003) · cites this paper as [19]
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- Authors
- Bowe, D. B., Kenney, N. J., Adereth, Y., & Maroulakou, I. G.
- Affiliations
- Medical University of South Carolina (US)
- Hampton University (US)
- Corresponding author
- Maroulakou, Ioanna G
- Venue
- Oncogene
- Published
- 2002-01-10
- Volume
- 21
- Issue
- 2
- Pages
- 291-298
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2080483972
- Cited by
- 61
- References
- 30
- Citations by year
- 2025: 2 · 2023: 1 · 2022: 1 · 2017: 5 · 2015: 4 · 2014: 5 · 2013: 3 · 2012: 2
- FWCI
- 2.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- HER2/neu, cyclin D1, cyclin E, mammary tumor growth, breast cancer, cell cycle regulation, receptor tyrosine kinase signaling
- MeSH terms
- Adenocarcinoma, Animals, Female, Kinetics, Mammary Neoplasms, Experimental, Suppression, Genetic, Signal Transduction, Mice, Knockout, Erb-b2 Receptor Tyrosine Kinases, Genes, erbB-2, Cyclin E, Cyclin D1, Mice
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