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08 06, 2021;16 (1): 14.

Understanding p53 tumour suppressor network.

Emanuele Panatta, Carlotta Zampieri, Gerry Melino, Ivano Amelio
Author Information
  1. Emanuele Panatta: Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy.
  2. Carlotta Zampieri: Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy.
  3. Gerry Melino: Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy. ORCID
  4. Ivano Amelio: Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy. ivano.amelio@uniroma2.it. ORCID
PMID: 34362419 DOI: 10.1186/s13062-021-00298-3

Abstract

The mutation of TP53 gene affects half of all human cancers, resulting in impairment of the regulation of several cellular functions, including cell cycle progression and cell death in response to genotoxic stress. In the recent years additional p53-mediated tumour suppression mechanisms have been described, questioning the contribution of its canonical pathway for tumour suppression. These include regulation of alternative cell death modalities (i.e. ferroptosis), cell metabolism and the emerging role in RNA stability. Here we briefly summarize our knowledge on p53 "canonical DNA damage response" and discuss the most relevant recent findings describing potential mechanistic explanation of p53-mediated tumour suppression.

Keywords

Cell death DNA damage Stress response Tumour suppression

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MeSH Term

Cell Division
DNA Damage
Genes, Tumor Suppressor
Genes, p53
Humans
Mutation
Neoplasms
Tumor Suppressor Protein p53

Chemicals

TP53 protein, human
Tumor Suppressor Protein p53
Journal Article Research Support, Non-U.S. Gov't
Article has an altmetric score of 1

Word Cloud

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