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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,...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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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. |
format | Online Article Text |
id | pubmed-8709944 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
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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