Genomic Instability: The Pivotal Role of Mutant P53 in Human CancersSilvia Di Agostino* and Giovanni Blandino
Translational Oncogenomic Unit, Molecular Medicine Area, Regina Elena National Cancer Institute, Rome 00144, Italy
- *Corresponding Author:
- Silvia Di Agostino
Translational Oncogenomic Unit
Molecular Medicine Area
Regina Elena National Cancer Institute
E-mail: [email protected]
Received date: January 11, 2016; Accepted date: February 13, 2016; Published date: February 18, 2016
Citation: Di Agostino S, Blandino G (2016) Genomic Instability: The Pivotal Role of Mutant p53 in Human Cancers. Chemo Open Access 5:191. doi:10.4172/2167-7700.1000191
Copyright: © 2016 Di Agostino S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The tumor suppressor p53 plays a critical role to preserve DNA fidelity from diverse insults through the regulation of cell-cycle checkpoints, DNA repair, senescence and apoptosis. The TP53 is altered in more than half of human cancers. This leads to the production of mutant p53 proteins that loose wild type p53 tumor suppression functions and concomitantly acquire new oncogenic deleterious features implicated in: increased cell proliferation, increased chemoresistance, disruption of tissue architecture, promotion of migration, invasion and metastasis and several other pro-oncogenic properties. Accumulating evidences suggest that mutant p53 proteins drastically perturb the residual genome-stabilizing mechanisms during cancer progression, thereby increasing genomic instability of mutant p53 carrying human cancers. In this commentary we briefly summarize the most important evidences suggesting that mutant p53 plays a relevant role in promoting genomic instability in human cancers.