Role of RUNX Family Transcription Factors in DNA Damage Response
Ann Sanoji Samarakkody1, Nah-Young Shin1, and Alan B. Cantor1,2,*
1Department of Pediatric Hematology-Oncology, Boston Children’s Hospital and Dana Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA, 2Harvard Stem Cell Institute, Cambridge, MA 02138, USA
Received December 5, 2019; Accepted December 12, 2019.; Published online February 6, 2020.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

ABSTRACT
Cells are constantly exposed to endogenous and exogenous stresses that can result in DNA damage. In response, they have evolved complex pathways to maintain genomic integrity. RUNX family transcription factors (RUNX1, RUNX2, and RUNX3 in mammals) are master regulators of development and differentiation, and are frequently dysregulated in cancer. A growing body of research also implicates RUNX proteins as regulators of the DNA damage response, often acting in conjunction with the p53 and Fanconi anemia pathways. In this review, we discuss the functional role and mechanisms involved in RUNX factor mediated response to DNA damage and other cellular stresses. We highlight the impact of these new findings on our understanding of cancer predisposition associated with RUNX factor dysregulation and their implications for designing novel approaches to prevent cancer formation in affected individuals.
Keywords: cancer, cell cycle arrest, DNA damage response, Fanconi anemia, p53, RUNX1, RUNX2, RUNX3, tumor suppressor


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31 January 2020 Volume 43,
Number 1, pp. 1~95

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