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11 08, 2021;16 (1): 23.

The p53 family member p73 in the regulation of cell stress response.

Julian M Rozenberg, Svetlana Zvereva, Aleksandra Dalina, Igor Blatov, Ilya Zubarev, Daniil Luppov, Alexander Bessmertnyi, Alexander Romanishin, Lamak Alsoulaiman, Vadim Kumeiko, Alexander Kagansky, Gerry Melino, Carlo Ganini, Nikolai A Barlev
Author Information
  1. Julian M Rozenberg: Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia. rozenbej@gmail.com. ORCID
  2. Svetlana Zvereva: Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
  3. Aleksandra Dalina: The Engelhardt Institute of Molecular Biology, Russian Academy of Science, Moscow, Russia.
  4. Igor Blatov: Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
  5. Ilya Zubarev: Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
  6. Daniil Luppov: Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
  7. Alexander Bessmertnyi: HSE University, Moscow, Russia.
  8. Alexander Romanishin: School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia.
  9. Lamak Alsoulaiman: Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
  10. Vadim Kumeiko: School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia.
  11. Alexander Kagansky: Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.
  12. Gerry Melino: Department of Medicine, University of Rome Tor Vergata, Rome, Italy.
  13. Carlo Ganini: Department of Medicine, University of Rome Tor Vergata, Rome, Italy.
  14. Nikolai A Barlev: Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia. nick.a.barlev@gmail.com.
PMID: 34749806 DOI: 10.1186/s13062-021-00307-5

Abstract

During oncogenesis, cells become unrestrictedly proliferative thereby altering the tissue homeostasis and resulting in subsequent hyperplasia. This process is paralleled by resumption of cell cycle, aberrant DNA repair and blunting the apoptotic program in response to DNA damage. In most human cancers these processes are associated with malfunctioning of tumor suppressor p53. Intriguingly, in some cases two other members of the p53 family of proteins, transcription factors p63 and p73, can compensate for loss of p53. Although both p63 and p73 can bind the same DNA sequences as p53 and their transcriptionally active isoforms are able to regulate the expression of p53-dependent genes, the strongest overlap with p53 functions was detected for p73. Surprisingly, unlike p53, the p73 is rarely lost or mutated in cancers. On the contrary, its inactive isoforms are often overexpressed in cancer. In this review, we discuss several lines of evidence that cancer cells develop various mechanisms to repress p73-mediated cell death. Moreover, p73 isoforms may promote cancer growth by enhancing an anti-oxidative response, the Warburg effect and by repressing senescence. Thus, we speculate that the role of p73 in tumorigenesis can be ambivalent and hence, requires new therapeutic strategies that would specifically repress the oncogenic functions of p73, while keeping its tumor suppressive properties intact.

Keywords

Cancer hallmarks Tumor suppressor p53 p73

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MeSH Term

DNA-Binding Proteins
Genes, Tumor Suppressor
Humans
Nuclear Proteins
Phosphoproteins
Trans-Activators
Tumor Protein p73
Tumor Suppressor Protein p53
Tumor Suppressor Proteins

Chemicals

DNA-Binding Proteins
Nuclear Proteins
Phosphoproteins
Trans-Activators
Tumor Protein p73
Tumor Suppressor Protein p53
Tumor Suppressor Proteins
Journal Article Research Support, Non-U.S. Gov't Review
Article has an altmetric score of 1

Word Cloud

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