Journal
CLINICAL CANCER RESEARCH
Volume 17, Issue 1, Pages 12-18Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1078-0432.CCR-10-0752
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Funding
- Doris Duke Charitable Foundation
- National Cancer Institute [R01CA105118]
- NATIONAL CANCER INSTITUTE [R01CA123415, R01CA105118] Funding Source: NIH RePORTER
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Phosphorylation of the cyclin-dependent kinase inhibitor p27 by upstream mitogenic signaling pathways regulates its stability, localization, and biological function. In human cancers, loss of the antiproliferative action of p27 can arise through reduced protein levels and/or cytoplasmic mislocalization, leading to increased cell proliferation and/or cell migration, respectively. Reduced p27 expression levels and p27 mislocalization have potential prognostic and therapeutic implications in various types of human cancers.This review highlights mechanisms of functional deregulation of p27 by oncogenic signaling that provide an important molecular rationale for pathway targeting in cancer treatment. Clin Cancer Res; 17( 1); 12-8. (C) 2010 AACR.
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