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

Autor:	Rozenberg JM; Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia. rozenbej@gmail.com., Zvereva S; Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia., Dalina A; The Engelhardt Institute of Molecular Biology, Russian Academy of Science, Moscow, Russia., Blatov I; Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia., Zubarev I; Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia., Luppov D; Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia., Bessmertnyi A; HSE University, Moscow, Russia., Romanishin A; School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia.; School of Life Sciences, Immanuel Kant Baltic Federal University, Kaliningrad, Russia., Alsoulaiman L; Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia., Kumeiko V; School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia., Kagansky A; Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia.; School of Biomedicine, Far Eastern Federal University, Vladivostok, Russia., Melino G; Department of Medicine, University of Rome Tor Vergata, Rome, Italy., Ganini C; Department of Medicine, University of Rome Tor Vergata, Rome, Italy., Barlev NA; Cell Signaling Regulation Laboratory, Moscow Institute of Physics and Technology, Dolgoprudny, Russia. nick.a.barlev@gmail.com.; Institute of Cytology, Russian Academy of Science, Saint-Petersburg, Russia. nick.a.barlev@gmail.com.
Jazyk:	angličtina
Zdroj:	Biology direct [Biol Direct] 2021 Nov 08; Vol. 16 (1), pp. 23. Date of Electronic Publication: 2021 Nov 08.
DOI:	10.1186/s13062-021-00307-5
Abstrakt:	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. (© 2021. The Author(s).)
Databáze:	MEDLINE
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