ArticleMolecular and cellular biology2001
Tumor-specific proteolytic processing of cyclin E generates hyperactive lower-molecular-weight forms.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 197 citations in OpenAlex.
- Functional Profiling of p53 and RB Cell Cycle Regulatory Proficiency Suggests Mechanism-Driven Molecular Stratification in Endometrial Carcinoma.Cancer research communications · 2025Article
- Natural Compounds as Protease Inhibitors in Therapeutic Focus on Cancer Therapy.Anti-cancer agents in medicinal chemistry · 2024Review
- Targeting cell-cycle machinery in cancer.Cancer cell · 2021Review
- LMW cyclin E and its novel catalytic partner CDK5 are therapeutic targets and prognostic biomarkers in salivary gland cancers.Oncogenesis · 2021Article
- Article
- The requirement for cyclin E in c-Myc overexpressing breast cancers.Cell cycle (Georgetown, Tex.) · 2020Article
- Molecular crosstalk between cancer and neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Targeting eukaryotic proteases for natural products-based drug development.Natural product reports · 2020Review
- Two unique HLA-A*0201 restricted peptides derived from cyclin E as immunotherapeutic targets in leukemia.Leukemia · 2020Article
- Article
- Cyclin E expression is associated with high levels of replication stress in triple-negative breast cancer.NPJ breast cancer · 2020Article
- Cyclin E: a potential treatment target to reverse cancer chemoresistance by regulating the cell cycle.American journal of translational research · 2020Review
- Cul3 regulates cyclin E1 protein abundance via a degron located within the N-terminal region of cyclin E.Journal of cell science · 2019Article
- Cyclin E mRNA: Assessing Cyclin-Dependent Kinase (CDK) Activation State to Elucidate Breast Cancer Resistance to CDK4/6 Inhibitors.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2019Article
- Primary neurons can enter M-phase.Scientific reports · 2019Article
- Low-Molecular-Weight Cyclin E in Human Cancer: Cellular Consequences and Opportunities for Targeted Therapies.Cancer research · 2018Review
- Structural insights into the functional diversity of the CDK-cyclin family.Open biology · 2018Review
- Neuropilin-1 mediates neutrophil elastase uptake and cross-presentation in breast cancer cells.The Journal of biological chemistry · 2017Article
- Cytoplasmic Cyclin E Predicts Recurrence in Patients with Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Cyclin E overexpression as a biomarker for combination treatment strategies in inflammatory breast cancer.Oncotarget · 2017Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Cyclin E is a G(1) cyclin essential for S-phase entry and has a profound role in oncogenesis. Previously this laboratory found that cyclin E is overexpressed and present in lower-molecular-weight (LMW) isoforms in breast cancer cells and tumor tissues compared to normal cells and tissues. Such alteration of cyclin E is linked to poor patient outcome. Here we report that the LMW forms of cyclin E are hyperactive biochemically and they can more readily induce G(1)-to-S progression in transfected normal cells than the full-length form of the protein can. Through biochemical and mutational analyses we have identified two proteolytically sensitive sites in the amino terminus of human cyclin E that are cleaved to generate the LMW isoforms found in tumor cells. Not only are the LMW forms of cyclin E functional, as they phosphorylate substrates such as histone H1 and GST-Rb, but also their activities are higher than the full-length cyclin E. These nuclear localized LMW forms of cyclin E are also biologically functional, as their overexpression in normal cells increases the ability of these cells to enter S and G(2)/M. Lastly, we show that cyclin E is selectively cleaved in vitro by the elastase class of serine proteases to generate LMW forms similar to those observed in tumor cells. These studies suggest that the defective entry into and exit from S phase by tumor cells is in part due to the proteolytic processing of cyclin E, which generates hyperactive LMW isoforms whose activities have been modified from that of the full-length protein.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.