ArticleOncogene1999
Cyclin E dependent kinase activity in human breast cancer in relation to cyclin E, p27 and p21 expression and retinoblastoma protein phosphorylation.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 46 citations in OpenAlex.
- Organic extract ofOncology letters · 2022Article
- TMED3 Promotes Proliferation and Migration in Breast Cancer Cells by Activating Wnt/β-Catenin Signaling.OncoTargets and therapy · 2020Article
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- Cyclin-dependent kinase inhibitors CIP1 (p21) and KIP1 (p27) in ovarian cancer.Journal of cancer research and clinical oncology · 2006Article
- Article
- Estrogen receptor beta inhibits 17beta-estradiol-stimulated proliferation of the breast cancer cell line T47D.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- p27 deregulation in breast cancer: prognostic significance and implications for therapy.Journal of mammary gland biology and neoplasia · 2004Review
- Deregulation of p27 by oncogenic signaling and its prognostic significance in breast cancer.Breast cancer research : BCR · 2004Review
- Cell cycle genes in a mouse mammary hyperplasia model.Journal of mammary gland biology and neoplasia · 2004Review
- Deregulation of cyclin E2 expression and associated kinase activity in primary breast tumors.Oncogene · 2002Article
- Article
- Overexpression of cyclin E in Mongolian gerbil with Helicobacter pylori-induced gastric precancerosis.World journal of gastroenterology · 2002Article
- Activation of cyclin E-dependent kinase activity in colorectal cancer.Digestive diseases and sciences · 2001Article
- Article
- The cyclin dependent kinase inhibitor p27 and its prognostic role in breast cancer.Breast cancer research : BCR · 2001Review
- Abnormal expression of p27kip1 protein in levator ani muscle of aging women with pelvic floor disorders - a relationship to the cellular differentiation and degeneration.BMC clinical pathology · 2001Article
- ErbB2 potentiates breast tumor proliferation through modulation of p27(Kip1)-Cdk2 complex formation: receptor overexpression does not determine growth dependency.Molecular and cellular biology · 2000Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cell cycle machinery is regulated by cyclin dependent kinases and sets of activating and inhibitory proteins. The G1-S control mechanism is often deregulated in tumours supposedly leading to increased kinase activity, phosphorylation of substrates and subsequent S phase entrance. Increased kinase activity has been proposed to be essential in cell cycle aberrations, but few studies have actually shown enhanced kinase activity related to specific cell cycle defects in primary tumours. In the present study we have determined the cyclin E dependent kinase activity (cyclin E(kinase)) in 59 primary breast cancers, using an H1-kinase assay, and related the activity to the expression of cyclin E, p27 and p21. In a subgroup of 48 tumours, we further characterized the association between cyclin E(kinase), in vivo phosphorylation of the retinoblastoma protein (pRb) and proliferation. The cyclin E(kinase) correlated significantly with cyclin E content and inversely with p27 and p21 expression. P27, but not p21, was associated with low cyclin E(kinase) in specimens with normal/low levels of cyclin E. At elevated cyclin E levels, suppression of cyclin E(kinase) seemed to require high levels of both p21 and p27. The cyclin E(kinase) correlated with the phosphorylation status of pRb as well as with proliferation. Surprisingly, pRb phosphorylation did not correlate with proliferation. Our results support that pRb is a substrate for cyclin E(kinase) in primary breast cancer and that deregulation of cyclin E and p27 act through increased CDK-kinase activity, but cyclin E associated events beside pRb phosphorylation might be rate-limiting for entrance into S phase.
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