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DNA polymerase β imbalance increases apoptosis and mutagenesis induced by oxidative stress
Author(s) -
Fréchet Mathilde,
Canitrot Yvan,
Cazaux Christophe,
Hoffmann Jean-Sébastien
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02834-4
Subject(s) - oxidative stress , polymerase , dna polymerase , mutagenesis , dna damage , dna polymerase beta , mutation , biology , dna repair , microbiology and biotechnology , poly adp ribose polymerase , oxidative phosphorylation , dna , genetics , gene , biochemistry , base excision repair
Oxidative stress has been proposed to be one of the major causes leading to the accumulation of mutation that is associated with the initiation and progression of cancers. Elevated expression of DNA polymerase β, an event found in many human tumors, has been shown to generate a mutator phenotype. Here, we demonstrated that overexpression of DNA polymerase β strengthens the mutagenicity of oxidative damages, concomitantly with a higher cellular sensitivity and increased apoptosis. Deregulated expression of DNA polymerase β could represent a predisposition factor for mutagenic effects of oxidative stress and thus have implication in the generation and/or evolution of cancer.