Cancer is caused by genetic changes that often arise following failure to accurately replicate the DNA. PCNA (proliferating-cell nuclear antigen) forms a ring around the DNA to facilitate and control DNA replication. Emerging evidence suggests that PCNA is at the very heart of many essential cellular processes, such as DNA replication, repair of DNA damage, chromatin structure maintenance, chromosome segregation and cell-cycle progression. Progression of the DNA replication forks can be blocked by DNA lesions, formed either by endogenous damage or by exogenous agents, for instance anticancer drugs. Cellular response often results in change of PCNA function triggered either by specific post-translational modification of PCNA (i.e. ubiquitylation) or by exchange of its interaction partners. This puts PCNA in a central position in determining the fate of the replication fork. In the present article, we review PCNA modifications and interaction partners, and how those influence the course of events at replication forks, which ultimately determines both tumour progression as well as the outcome of anticancer treatment.
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June 2009
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Conference Article|
May 20 2009
PCNA on the crossroad of cancer
Ivaylo Stoimenov;
Ivaylo Stoimenov
*Department of Genetics, Microbiology and Toxicology, Stockholm University, S-106 91 Stockholm, Sweden
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Thomas Helleday
Thomas Helleday
1
*Department of Genetics, Microbiology and Toxicology, Stockholm University, S-106 91 Stockholm, Sweden
†Gray Institute for Radiation Oncology and Biology, Old Road Campus Research Building, Roosevelt Drive, University of Oxford, Oxford OX3 7DQ, U.K.
1To whom correspondence should be addressed (email thomas.helleday@rob.ox.ac.uk).
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Publisher: Portland Press Ltd
Received:
December 09 2008
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2009 Biochemical Society
2009
Biochem Soc Trans (2009) 37 (3): 605–613.
Article history
Received:
December 09 2008
Citation
Ivaylo Stoimenov, Thomas Helleday; PCNA on the crossroad of cancer. Biochem Soc Trans 1 June 2009; 37 (3): 605–613. doi: https://doi.org/10.1042/BST0370605
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