NDLI: EZH2 is a marker of aggressive breast cancer and promotes neoplastic transformation of breast epithelial cells.

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EZH2 is a marker of aggressive breast cancer and promotes neoplastic transformation of breast epithelial cells.

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EZH2 is a marker of aggressive breast cancer and promotes neoplastic transformation of breast epithelial cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Ghosh, Debashis Otte, Arie P. Livant, Donna Cao, Qi Rubin, Mark A. Sewalt, Richard G. A. B. Sabel, Michael S. Kleer, Celina G. Weiss, Stephen J. Ota, Ichiro Chinnaiyan, Arul M. Shen, Ronglai Hayes, Daniel F. Tomlins, Scott A. Varambally, Sooryanarayana
Description	Author Affiliation: Kleer CG ( Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA. kleer@umich.edu);
Abstract	The Polycomb Group Protein EZH2 is a transcriptional repressor involved in controlling cellular memory and has been linked to aggressive prostate cancer. Here we investigate the functional role of EZH2 in cancer cell invasion and breast cancer progression. EZH2 transcript and protein were consistently elevated in invasive breast carcinoma compared with normal breast epithelia. Tissue microarray analysis, which included 917 samples from 280 patients, demonstrated that EZH2 protein levels were strongly associated with breast cancer aggressiveness. Overexpression of EZH2 in immortalized human mammary epithelial cell lines promotes anchorage-independent growth and cell invasion. EZH2-mediated cell invasion required an intact SET domain and histone deacetylase activity. This study provides compelling evidence for a functional link between dysregulated cellular memory, transcriptional repression, and neoplastic transformation.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	20
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Breast Neoplasms Pathology Breast Cell Transformation, Neoplastic Epithelial Cells Proteins Physiology Metabolism DNA-Binding Proteins Immunohistochemistry Polycomb Repressive Complex 2 Polymerase Chain Reaction Genetics RNA, Messenger Transcription Factors Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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