Importance of Ezh2 polycomb protein in tumorigenesis process interfering with the pathway of growth suppressive key elements

• Published in: Journal of cellular physiology Vol. 214; no. 2; pp. 295 - 300
• Main Authors: Tonini, Tiziana, D'Andrilli, Giuseppina, Fucito, Alfredo, Gaspa, Leonardo, Bagella, Luigi
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01-02-2008
• Subjects: Animals; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; Cell Transformation, Neoplastic - genetics; Cell Transformation, Neoplastic - metabolism; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Enhancer of Zeste Homolog 2 Protein; Female; Histone Deacetylases - metabolism; Histone-Lysine N-Methyltransferase; Humans; Male; Models, Genetic; Neoplasms - genetics; Neoplasms - metabolism; Neoplasms - pathology; Polycomb Repressive Complex 2; Prostatic Neoplasms - genetics; Prostatic Neoplasms - metabolism; Prostatic Neoplasms - pathology; Proteins - genetics; Proteins - metabolism; Repressor Proteins - genetics; Repressor Proteins - metabolism; Retinoblastoma Protein - genetics; Retinoblastoma Protein - metabolism; Retinoblastoma-Like Protein p107 - genetics; Retinoblastoma-Like Protein p107 - metabolism; Retinoblastoma-Like Protein p130 - genetics; Retinoblastoma-Like Protein p130 - metabolism; Transcription Factors - genetics; Transcription Factors - metabolism
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.21241

An understanding of the mechanisms that uncover the dynamic changes in the distribution of the chromatin modifying enzymes and regulatory proteins on their target loci could provide further insight into the phenomenon of malignant transformation. Based on the current available data, it seems more and more clear that an abnormal expression of Ezh2, a member of the Polycomb group (PcG) protein, may be involved in the tumorigenesis process, in addition, different studies identify Ezh2 as a potential marker that distinguish aggressive prostate and breast cancer from indolent one. Recent investigation show that ectopic expression of Ezh2 provides proliferative advantage to primary cells through interaction with the pathways of key elements that control cell growth arrest and differentiation, like members of the retinoblastoma (Rb) family. Here, we outline how these pathways converge and we review the recent advances on the molecular mechanisms that promote cell cycle progression through deregulation of Ezh2 protein level, providing novel links between cancer progression and chromatin remodeling machineries. J. Cell. Physiol. 214: 295–300, 2008. © 2007 Wiley‐Liss, Inc.