Abstract
Cyclin E, a key mediator of entry into the cell division cycle, is expressed abundantly in many breast cancers. However, amplification of the cognate gene is observed rarely, leaving the responsible mechanism(s) and its importance in tumorigenesis in doubt. In a recent report, Steve Reed's lab demonstrates that hCdc4/Fbw7 targets cyclin E for ubiquitin-mediated proteolysis and is mutant in a breast cancer cell line with high cyclin E levels. Independent work demonstrates that a Drosophila hCdc4 homologue constrains cyclin E expression in vivo. These results suggest that lesions in protein degradation pathways may contribute to cyclin E deregulation in breast cancer.
MeSH Terms
Breast Neoplasms/metabolism,pathology
Cell Cycle
Cell Cycle Proteins/genetics,physiology
Cell Line, Transformed
Cyclins/metabolism
F-Box Proteins
F-Box-WD Repeat-Containing Protein 7
Female
Fungal Proteins/metabolism
Gene Expression Regulation, Neoplastic
Genes, Tumor Suppressor
Humans
Neoplasm Proteins/metabolism
Phosphorylation
Protein Processing, Post-Translational
Saccharomyces cerevisiae/cytology,metabolism
Saccharomyces cerevisiae Proteins/genetics,physiology
Tumor Cells, Cultured
Ubiquitin-Protein Ligases
Chemicals
CDC4 protein, S cerevisiae
Cell Cycle Proteins
Cyclins
F-Box Proteins
F-Box-WD Repeat-Containing Protein 7
FBXW7 protein, human
Fungal Proteins
Neoplasm Proteins
Saccharomyces cerevisiae Proteins
Ubiquitin-Protein Ligases
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Enders Greg H
Penn/GI Division, Suite 600/CRB, 415 Curie Boulevard, Philadelphia, PA 19104-6144, USA.
[email protected]
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