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Carcinogenesis Advance Access originally published online on November 28, 2007
Carcinogenesis 2008 29(2):237-243; doi:10.1093/carcin/bgm268
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

CDC6: from DNA replication to cell cycle checkpoints and oncogenesis

Luis R. Borlado and Juan Méndez*

DNA replication Group, Molecular Oncology Programme, Spanish National Cancer Research Centre, Melchor Fernández Almagro 3, E-28029 Madrid, Spain

* To whom correspondence should be addressed. Tel: +34 91 732 8008; Fax: +34 91 732 8033; Email: jmendez{at}cnio.es

Cell division cycle 6 (CDC6) is an essential regulator of DNA replication in eukaryotic cells. Its best-characterized function is the assembly of prereplicative complexes at origins of replication during the G1 phase of the cell division cycle. However, CDC6 also plays important roles in the activation and maintenance of the checkpoint mechanisms that coordinate S phase and mitosis, and recent studies have unveiled its proto-oncogenic activity. CDC6 overexpression interferes with the expression of INK4/ARF tumor suppressor genes through a mechanism involving the epigenetic modification of chromatin at the INK4/ARF locus. In addition, CDC6 overexpression in primary cells may promote DNA hyperreplication and induce a senescence response similar to that caused by oncogene activation. These findings indicate that deregulation of CDC6 expression in human cells poses a serious risk of carcinogenesis.

Abbreviations: CDC6, cell division cycle 6; CDK, cyclin-dependent kinase; DDR, DNA damage response; MCM, minichromosome maintenance; ORC, origin recognition complex; pre-RC, pre-replication complex

Received September 11, 2007; revised November 14, 2007; accepted November 18, 2007.


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