• Open Access

PolyADP-ribosylation and cancer


  • Masanao Miwa,

    Corresponding author
    1. Faculty of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura-cho Nagahama, Shiga 526-0829;
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  • Mitsuko Masutani

    1. ADP-ribosylation in Oncology Project, Biochemistry Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
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To whom correspondence should be addressed. E-mail: m_miwa@nagahama-i-bio.ac.jp


The polyADP-ribosylation reaction results in a unique post-translational modification involved in various cellular processes and conditions, including DNA repair, transcriptional control, genomic stability, cell death and transformation. The existence of 17 members of the poly(ADP-ribose) polymerase (PARP) family has so far been documented, with overlapping functional consequences. PARP-1 is known to be involved in DNA base excision repair and this explains the susceptibility spectrum of PARP-1 knockout animals to genotoxic carcinogens. The fact that centrosome amplification is induced by a non-genotoxic inhibitor of PARP and in PARP-1 knockout mouse cells, is in line with aneuploidy, which is frequent in cancers. Genetically engineered animal models have revealed that PARP-1 and VPARP impact carcinogenesis. Furthermore, accumulating experimental evidence supports the utility of PARP and PARG inhibitors in cancer therapy and several clinical trials are now ongoing. Increasing NAD+ levels by pharmacological supplementation with niacin has also been found to exert preventive effects against cancer. In the present review, recent research progress on polyADP-ribosylation related to neoplasia is summarized and discussed. (Cancer Sci 2007; 98: 1528–1535)