REVIEW: Translesion DNA Synthesis and Carcinogenesis

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E. S. Shilkin¹, E. O. Boldinova¹, A. D. Stolyarenko¹, R. I. Goncharova², R. N. Chuprov-Netochin³, R. F. Khairullin⁴, M. P. Smal^2,a*, and A. V. Makarova^1,b*

¹Institute of Molecular Genetics, Russian Academy of Sciences, 123182 Moscow, Russia

²Institute of Genetics and Cytology, National Academy of Sciences of Belarus, 220072 Minsk, Republic of Belarus

³Moscow Institute of Physics and Technology, 141701 Dolgoprudny, Moscow Region, Russia

⁴Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, 420012 Kazan, Russia

^* To whom correspondence should be addressed.

Received December 4, 2019; Revised February 20, 2020; Accepted February 20, 2020

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Tens of thousands of DNA lesions are formed in mammalian cells each day. DNA translesion synthesis is the main mechanism of cell defense against unrepaired DNA lesions. DNA polymerases iota (Pol ι), eta (Pol η), kappa (Pol κ), and zeta (Pol ζ) have active sites that are less stringent toward the DNA template structure and efficiently incorporate nucleotides opposite DNA lesions. However, these polymerases display low accuracy of DNA synthesis and can introduce mutations in genomic DNA. Impaired functioning of these enzymes can lead to an increased risk of cancer.

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KEY WORDS: translesion DNA synthesis, DNA damage, mutagenesis, carcinogenesis

DOI: 10.1134/S0006297920040033

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