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p53 signaling in cancer progression and therapy

The p53 protein is a transcription factor known as the "guardian of the genome" because of its critical function in preserving genomic integrity. The TP53 gene is mutated in approximately half of all human malignancies, including those of the breast, colon, lung, liver, prostate, bladder,...

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Autores principales: Marei, Hany E., Althani, Asmaa, Afifi, Nahla, Hasan, Anwarul, Caceci, Thomas, Pozzoli, Giacomo, Morrione, Andrea, Giordano, Antonio, Cenciarelli, Carlo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8709944/
https://www.ncbi.nlm.nih.gov/pubmed/34952583
http://dx.doi.org/10.1186/s12935-021-02396-8
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author Marei, Hany E.
Althani, Asmaa
Afifi, Nahla
Hasan, Anwarul
Caceci, Thomas
Pozzoli, Giacomo
Morrione, Andrea
Giordano, Antonio
Cenciarelli, Carlo
author_facet Marei, Hany E.
Althani, Asmaa
Afifi, Nahla
Hasan, Anwarul
Caceci, Thomas
Pozzoli, Giacomo
Morrione, Andrea
Giordano, Antonio
Cenciarelli, Carlo
author_sort Marei, Hany E.
collection PubMed
description The p53 protein is a transcription factor known as the "guardian of the genome" because of its critical function in preserving genomic integrity. The TP53 gene is mutated in approximately half of all human malignancies, including those of the breast, colon, lung, liver, prostate, bladder, and skin. When DNA damage occurs, the TP53 gene on human chromosome 17 stops the cell cycle. If p53 protein is mutated, the cell cycle is unrestricted and the damaged DNA is replicated, resulting in uncontrolled cell proliferation and cancer tumours. Tumor-associated p53 mutations are usually associated with phenotypes distinct from those caused by the loss of the tumor-suppressing function exerted by wild-type p53protein. Many of these mutant p53 proteins have oncogenic characteristics, and therefore modulate the ability of cancer cells to proliferate, escape apoptosis, invade and metastasize. Because p53 deficiency is so common in human cancer, this protein is an excellent option for cancer treatment. In this review, we will discuss some of the molecular pathways by which mutant p53 proteins might perform their oncogenic activities, as well as prospective treatment methods based on restoring tumor suppressive p53 functions.
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spelling pubmed-87099442022-01-05 p53 signaling in cancer progression and therapy Marei, Hany E. Althani, Asmaa Afifi, Nahla Hasan, Anwarul Caceci, Thomas Pozzoli, Giacomo Morrione, Andrea Giordano, Antonio Cenciarelli, Carlo Cancer Cell Int Review The p53 protein is a transcription factor known as the "guardian of the genome" because of its critical function in preserving genomic integrity. The TP53 gene is mutated in approximately half of all human malignancies, including those of the breast, colon, lung, liver, prostate, bladder, and skin. When DNA damage occurs, the TP53 gene on human chromosome 17 stops the cell cycle. If p53 protein is mutated, the cell cycle is unrestricted and the damaged DNA is replicated, resulting in uncontrolled cell proliferation and cancer tumours. Tumor-associated p53 mutations are usually associated with phenotypes distinct from those caused by the loss of the tumor-suppressing function exerted by wild-type p53protein. Many of these mutant p53 proteins have oncogenic characteristics, and therefore modulate the ability of cancer cells to proliferate, escape apoptosis, invade and metastasize. Because p53 deficiency is so common in human cancer, this protein is an excellent option for cancer treatment. In this review, we will discuss some of the molecular pathways by which mutant p53 proteins might perform their oncogenic activities, as well as prospective treatment methods based on restoring tumor suppressive p53 functions. BioMed Central 2021-12-24 /pmc/articles/PMC8709944/ /pubmed/34952583 http://dx.doi.org/10.1186/s12935-021-02396-8 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Marei, Hany E.
Althani, Asmaa
Afifi, Nahla
Hasan, Anwarul
Caceci, Thomas
Pozzoli, Giacomo
Morrione, Andrea
Giordano, Antonio
Cenciarelli, Carlo
p53 signaling in cancer progression and therapy
title p53 signaling in cancer progression and therapy
title_full p53 signaling in cancer progression and therapy
title_fullStr p53 signaling in cancer progression and therapy
title_full_unstemmed p53 signaling in cancer progression and therapy
title_short p53 signaling in cancer progression and therapy
title_sort p53 signaling in cancer progression and therapy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8709944/
https://www.ncbi.nlm.nih.gov/pubmed/34952583
http://dx.doi.org/10.1186/s12935-021-02396-8
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