The hallmarks of CDKN1C (p57, KIP2) in cancer.

Abstract

Cyclin-dependent kinase inhibitor 1C CDKN1C (p57(KIP2)) regulates several hallmarks of cancer, including apoptosis, cell invasion and metastasis, tumor differentiation and angiogenesis. p57(KIP2) is generally not mutated in cancer, but its expression is downregulated through epigenetic changes such as DNA methylation and repressive histone marks at the promoter. This opens up possibilities for therapeutic intervention through reactivation of p57(KIP2) gene expression. Furthermore, p57(KIP2) has been tested as a prognostic factor for many types of cancer, even differentiating between early and late stage cancer. In this review, the multifunctional tumor suppressor capabilities of p57(KIP2), the mechanisms of p57(KIP2) transcriptional repression in cancer, and the therapeutic potential of reactivation of p57(KIP2) protein expression will be discussed.

• Authors: Edel Kavanagh, Bertrand Joseph
• Journal: Biochimica et biophysica acta (Biochim Biophys Acta) Vol. 1816 Issue 1 Pg. 50-6 (Aug 2011) ISSN: 0006-3002 [Print] Netherlands
• PMID: 21447370 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: 2011 Elsevier B.V. All rights reserved.

Chemical References

• CDKN1C protein, human
• Cyclin-Dependent Kinase Inhibitor p57

Topics

• Animals
• Cell Differentiation
• Cell Proliferation
• Cyclin-Dependent Kinase Inhibitor p57 (physiology)
• Humans
• Neoplasm Invasiveness
• Neoplasms (etiology, pathology, therapy)