Oncogenic RUNX3: A Link between p53 Deficiency and MYC Dysregulation
Yuki Date1,2 and Kosei Ito1,*
1Department of Molecular Bone Biology, Graduate School of Biomedical Sciences, Nagasaki University, Nagasaki 852-8588, Japan, 2Japan Society for the Promotion of Science, Tokyo 102-0083, Japan
Received November 24, 2019; Accepted December 12, 2019.; Published online January 23, 2020.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

The RUNX transcription factors serve as master regulators of development and are frequently dysregulated in human cancers. Among the three family members, RUNX3 is the least studied, and has long been considered to be a tumorsuppressor gene in human cancers. This idea is mainly based on the observation that RUNX3 is inactivated by genetic/ epigenetic alterations or protein mislocalization during the initiation of tumorigenesis. Recently, this paradigm has been challenged, as several lines of evidence have shown that RUNX3 is upregulated over the course of tumor development. Resolving this paradox and understanding how a single gene can exhibit both oncogenic and tumorsuppressive properties is essential for successful drug targeting of RUNX. We propose a simple explanation for the duality of RUNX3: p53 status. In this model, p53 deficiency causes RUNX3 to become an oncogene, resulting in aberrant upregulation of MYC.
Keywords: c-Myc, p53, RUNX3

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

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