| First Author | Miwa M | Year | 2007 |
| Journal | Cancer Sci | Volume | 98 |
| Issue | 10 | Pages | 1528-35 |
| PubMed ID | 17645773 | Mgi Jnum | J:138108 |
| Mgi Id | MGI:3804175 | Doi | 10.1111/j.1349-7006.2007.00567.x |
| Citation | Miwa M, et al. (2007) PolyADP-ribosylation and cancer. Cancer Sci 98(10):1528-35 |
| abstractText | 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. |
