Research Article
Received: 3 March 2009; Accepted: 22 April 2009
10.1002/emmm.200900022 About DOI
Heterochromatin protein 1  : a hallmark of cell proliferation relevant to clinical oncology |
| Leanne De Koning 1, Alexia Savignoni 2, Charlène Boumendil 1, Haniya Rehman 1, Bernard Asselain 2, Xavier Sastre-Garau 3, Geneviève Almouzni 1 * |
| 1Laboratory of Nuclear Dynamics and Genome Plasticity (UMR218), Institut Curie/CNRS/UPMC, 26 rue d'Ulm, 75248, Paris cedex 05, France 2Department of Biostatistics, Institut Curie, 26 rue d'Ulm, 75248, Paris cedex 05, France 3Department of Pathology, Institut Curie, 26 rue d'Ulm, 75248, Paris cedex 05, France |
| email: Geneviève Almouzni (Genevieve.Almouzni@curie.fr) |
*Correspondence to Geneviève Almouzni, Tel: 0033-156246701; Fax: 0033-146333016
| Keywords |
| cancer cell cycle heterochromatin HP1 proliferation |
| Abstract |
Mammalian cells contain three closely related heterochromatin protein 1 (HP1) isoforms, HP1 ,  and  , which, by analogy to their unique counterpart in Schizosaccharomyces pombe, have been implicated in gene silencing, genome stability and chromosome segregation. However, the individual importance of each isoform during normal cell cycle and disease has remained an unresolved issue. Here, we reveal that HP1 shows a proliferation-dependent regulation, which neither HP1 nor display. During transient cell cycle exit, the HP1 mRNA and protein levels diminish. Transient depletion of HP1, but not HP1 or , in tumoural and primary human cells leads to defects in chromosome segregation. Notably, analysis of an annotated collection of samples derived from carcinomas reveals an overexpression of HP1 mRNA and protein, which correlates with clinical data and disease outcome. Our results unveil a specific expression pattern for the HP1 isoform, suggesting a unique function related to cell division and tumour growth. The overexpression of HP1 constitutes a new example of a potential epigenetic contribution to tumourigenesis that is of clinical interest for cancer prognosis. |
Received: 3 March 2009; Accepted: 22 April 2009
| Digital Object Identifier (DOI) |
10.1002/emmm.200900022 About DOI
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