The Role of MIZ-1 in MYC-Dependent Tumorigenesis
Open Access
- 1 December 2013
- journal article
- review article
- Published by Cold Spring Harbor Laboratory in Cold Spring Harbor Perspectives in Medicine
- Vol. 3 (12), a014290
- https://doi.org/10.1101/cshperspect.a014290
Abstract
A hallmark of MYC-transformed cells is their aberrant response to antimitogenic signals. Key examples include the inability of MYC-transformed cells to arrest proliferation in response to antimitogenic signals such as TGF-β or DNA damage and their inability to differentiate into adipocytes in response to hormonal stimuli. Given the plethora of antimitogenic signals to which a tumor cell is exposed, it is likely that the ability to confer resistance to these signals is central to the transforming properties of MYC in vivo. At the same time, the inability of MYC-transformed cells to halt cell-cycle progression on stress may establish a dependence on mutations that impair or disable apoptosis. We propose that the interaction of MYC with the zinc finger protein MIZ-1 mediates resistance to antimitogenic signals. In contrast to other interactions of MYC, there is currently little evidence that MIZ-1 associates with MYC in normal, unperturbed cells. The functional interaction of both proteins becomes apparent at oncogenic expression levels of MYC and association with MIZ-1 mediates both oncogenic functions of MYC as well as tumor-suppressive responses to oncogenic levels of MYC.Keywords
This publication has 56 references indexed in Scilit:
- MYC DegradationCold Spring Harbor Perspectives in Medicine, 2014
- An Overview of MYC and Its InteractomeCold Spring Harbor Perspectives in Medicine, 2014
- Mule/Huwe1/Arf-BP1 suppresses Ras-driven tumorigenesis by preventing c-Myc/Miz1-mediated down-regulation of p21 and p15Genes & Development, 2013
- Physical Interaction between MYCN Oncogene and Polycomb Repressive Complex 2 (PRC2) in NeuroblastomaJournal of Biological Chemistry, 2013
- Nucleophosmin interacts directly with c-Myc and controls c-Myc-induced hyperproliferation and transformationProceedings of the National Academy of Sciences, 2008
- Miz1 and HectH9 regulate the stability of the checkpoint protein, TopBP1The EMBO Journal, 2008
- Modelling Myc inhibition as a cancer therapyNature, 2008
- The Quest for the1p36Tumor SuppressorCancer Research, 2008
- A Beta-Sheet Interaction Interface Directs the Tetramerisation of the Miz-1 POZ DomainJournal of Molecular Biology, 2007
- Repression of p15INK4b expression by Myc through association with Miz-1Nature, 2001