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Role of Poly-ADP-Ribosylation in Cancer Development

  • Chapter
Poly(ADP-Ribosyl)ation

Part of the book series: Molecular Biology Intelligence Unit ((MBIU))

Abstract

Elucidation of the relationship between poly-ADP-ribosylation and carcinogenesis has markedly progressed by the recent development of knockout or transgenic mice models of poly(ADP-ribose) polymerase (Parp)-1, Parp-2, and poly(ADP-ribose) glycohydrolase (Parg). Parp-1 is involved in base excision repair (BER), single- and |double-strand break repair, and chromosomal stability. These multiple functions explain why Parp-1 deficiency enhances carcinogenesis induced by alkylating agents and that in aged animals. Parp-1 is also involved in transcriptional regulation through protein-protein interaction as a coactivator and/or poly-ADP-ribosylation reaction and is possibly involved in epigenetic alteration during carcinogenesis and modulation of tumor phenotypes. Parp-1-dependent cell-death accompanying NAD depletion may be another important issue in carcinogenesis because this process could lead to the selection of Parp-1 deficient cells due to their survival advantage during cancer growth. The relationship of Parp-2, Parp-3, tankyrase and Parg with carcinogenesis is also discussed.

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Authors and Affiliations

  1. Biochemistry Division, National Cancer Center Research Institute, Tokyo, Japan

    Mitsuko Masutani, Akemi Gunji, Hitoshi Nakagama & Takashi Sugimura

  2. Department of Oncological Pathology, Cancer Center, Nara Medical University, Nara, Japan

    Masahiro Tsutsumi

  3. Department of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

    Kumiko Ogawa & Tomoyuki Shirai

  4. Chugai Research Institute for Medical Science, Inc., Shizuoka, Japan

    Nobuo Kamada & Kou-ichi Jishage

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Masutani, M. et al. (2006). Role of Poly-ADP-Ribosylation in Cancer Development. In: Poly(ADP-Ribosyl)ation. Molecular Biology Intelligence Unit. Springer, Boston, MA. https://doi.org/10.1007/0-387-36005-0_17

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