RUNX Family Participates in the Regulation of p53-Dependent DNA Damage ResponseReport as inadecuate




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International Journal of GenomicsVolume 2013 2013, Article ID 271347, 12 pages

Review Article

Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuohku, Chiba 260-8717, Japan

Laboratory of Innovative Cancer Therapeutics, Chiba Cancer Center Research Institute, Chiba 260-8717, Japan

Laboratory of Cancer Genetics, Chiba Cancer Center Research Institute, Chiba 260-8717, Japan

Received 18 June 2013; Accepted 1 August 2013

Academic Editor: Andreyan Osipov

Copyright © 2013 Toshinori Ozaki et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

A proper DNA damage response DDR, which monitors and maintains the genomic integrity, has been considered to be a critical barrier against genetic alterations to prevent tumor initiation and progression. The representative tumor suppressor p53 plays an important role in the regulation of DNA damage response. When cells receive DNA damage, p53 is quickly activated and induces cell cycle arrest and-or apoptotic cell death through transactivating its target genes implicated in the promotion of cell cycle arrest and-or apoptotic cell death such as p21

, BAX, and PUMA. Accumulating evidence strongly suggests that DNA damage-mediated activation as well as induction of p53 is regulated by posttranslational modifications and also by protein-protein interaction. Loss of p53 activity confers growth advantage and ensures survival in cancer cells by inhibiting apoptotic response required for tumor suppression. RUNX family, which is composed of RUNX1, RUNX2, and RUNX3, is a sequence-specific transcription factor and is closely involved in a variety of cellular processes including development, differentiation, and-or tumorigenesis. In this review, we describe a background of p53 and a functional collaboration between p53 and RUNX family in response to DNA damage.





Author: Toshinori Ozaki, Akira Nakagawara, and Hiroki Nagase

Source: https://www.hindawi.com/



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