Abstract
The tumor suppressor and transcription factor p53 plays critical roles in tumor prevention by orchestrating a wide variety of cellular responses, including damaged cell apoptosis, maintenance of genomic stability, inhibition of angiogenesis, and regulation of cell metabolism and tumor microenvironment. TP53 is one of the most commonly deregulated genes in cancer. The p53-ARF-MDM2 pathway is deregulated in 84% of glioblastoma (GBM) patients and 94% of GBM cell lines. Deregulated p53 pathway components have been implicated in GBM cell invasion, migration, proliferation, evasion of apoptosis, and cancer cell stemness. These pathway components are also regulated by various microRNAs and long non-coding RNAs. TP53 mutations in GBM are mostly point mutations that lead to a high expression of a gain of function (GOF) oncogenic variants of the p53 protein. These relatively understudied GOF p53 mutants promote GBM malignancy, possibly by acting as transcription factors on a set of genes other than those regulated by wild type p53. Their expression correlates with worse prognosis, highlighting their potential importance as markers and targets for GBM therapy. Understanding mutant p53 functions led to the development of novel approaches to restore p53 activity or promote mutant p53 degradation for future GBM therapies.
Highlights
The TP53 gene is located on human chromosome 17p13.1
ARF deletion is correlated with overexpression of tectonic family member 1 (TCTN1), a protein involved in a diverse range of cellular processes, including promotion of GBM cell proliferation
CDKN2A/ARF loss has not been shown to correlate with GBM prognosis and/or survival [27,32,33,34]
Summary
The TP53 gene is located on human chromosome 17p13.1. It encodes the p53 protein that consists of 393 amino acids (https://genome.ucsc.edu/). Evidence has shown that p53 is an important regulator p53 have revealed additional roles beyond gene transcription regulation and protectionofofcellular genome metabolism, stemness, autophagy, invasion, metastasis, microenvironment, and immunity [6,8,9]. Evidence has shown that p53 is an important regulator of cellular metabolism, Glioblastoma (GBM; grade IV glioma) is the most common and most deadly primary malignant stemness, autophagy, invasion, metastasis, microenvironment, and immunity [6,8,9]. Glioblastoma (GBM; grade IV glioma) is the most common and most deadly primary malignant treatment [10]. >90% TP53 mutations in co-occurrence with IDH1 mutations [14] Primary their differing mutational patterns: proneural, mesenchymal, neural, and classical [15]. We summarize the current understanding of p53 in GBM
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