The role of the TP73 gene and its transcripts in neuro-oncology

Abstract

Protein p73 is a member of the p53 protein family that can induce cell cycle arrest or apoptosis by the activation of p53-responsive genes as well as p53-independent pathways. Alternative promoter usage, together with differential splicing of the C-terminal exons, forms several distinct mRNAs that are translated into corresponding protein isoforms containing different domains. While TAp73 isoforms respond to genotoxic stress in a manner similar to tumor suppressor p53, ΔTAp73 isoforms inhibit apoptosis during normal development and in cancer cell lines. Thus, the impact of p73 on tumorigenesis depends on a subtle balance between tumor-promoting and- suppressing isoforms. Due to the structural homology between p53 and p73, a subtle balance among p53 family members and their isoforms could influence glioma cell evolution toward malignancy. Thus, the p73 status has to be considered when studying the regulatory role of p53 protein in gliomagenesis. The presented review summarizes recent knowledge about the issue of p73 and its isoforms with respect to neuro-oncology research.

Keywords::

• gliomagenesis
• isoforms
• TP73 gene
• p73 protein

Declaration of interest: The author reports no conflict of interest. The author alone is responsible for the content and writing of the paper.

Supported by the European Regional Development Fund - Project FNUSA-ICRC (No. CZ.1.05/1.1.00/02.0123) and the Ministry of Health of the Czech Republic grant No. NT14120.