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Deubiquitinating Enzyme-Mediated Signaling Networks in Cancer Stem Cells
SIMPLE SUMMARY: Cancer stem cells (CSCs) have both the capacity for self-renewal and the potential to differentiate and contribute to multiple tumor properties. The function of CSCs can be regulated by well-balanced process of ubiquitination and deubiquitination of proteins related to the specific s...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7694198/ https://www.ncbi.nlm.nih.gov/pubmed/33158118 http://dx.doi.org/10.3390/cancers12113253 |
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author | Kaushal, Kamini Ramakrishna, Suresh |
author_facet | Kaushal, Kamini Ramakrishna, Suresh |
author_sort | Kaushal, Kamini |
collection | PubMed |
description | SIMPLE SUMMARY: Cancer stem cells (CSCs) have both the capacity for self-renewal and the potential to differentiate and contribute to multiple tumor properties. The function of CSCs can be regulated by well-balanced process of ubiquitination and deubiquitination of proteins related to the specific stemness of the cells executing various stem cell fate choices. Growing evidence suggests that the involvement of deubiquitinating enzymes (DUBs) in altering several signaling pathways leading to survival of CSCs. In this review, we have compiled all the evidences of DUBs and summarized its role in regulating several signaling network in cancer stem cells. ABSTRACT: Cancer stem cells (CSCs) have both the capacity for self-renewal and the potential to differentiate and contribute to multiple tumor properties, such as recurrence, metastasis, heterogeneity, multidrug resistance, and radiation resistance. Thus, CSCs are considered to be promising therapeutic targets for cancer therapy. The function of CSCs can be regulated by ubiquitination and deubiquitination of proteins related to the specific stemness of the cells executing various stem cell fate choices. To regulate the balance between ubiquitination and deubiquitination processes, the disassembly of ubiquitin chains from specific substrates by deubiquitinating enzymes (DUBs) is crucial. Several key developmental and signaling pathways have been shown to play essential roles in this regulation. Growing evidence suggests that overactive or abnormal signaling within and among these pathways may contribute to the survival of CSCs. These signaling pathways have been experimentally shown to mediate various stem cell properties, such as self-renewal, cell fate decisions, survival, proliferation, and differentiation. In this review, we focus on the DUBs involved in CSCs signaling pathways, which are vital in regulating their stem-cell fate determination. |
format | Online Article Text |
id | pubmed-7694198 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-76941982020-11-28 Deubiquitinating Enzyme-Mediated Signaling Networks in Cancer Stem Cells Kaushal, Kamini Ramakrishna, Suresh Cancers (Basel) Review SIMPLE SUMMARY: Cancer stem cells (CSCs) have both the capacity for self-renewal and the potential to differentiate and contribute to multiple tumor properties. The function of CSCs can be regulated by well-balanced process of ubiquitination and deubiquitination of proteins related to the specific stemness of the cells executing various stem cell fate choices. Growing evidence suggests that the involvement of deubiquitinating enzymes (DUBs) in altering several signaling pathways leading to survival of CSCs. In this review, we have compiled all the evidences of DUBs and summarized its role in regulating several signaling network in cancer stem cells. ABSTRACT: Cancer stem cells (CSCs) have both the capacity for self-renewal and the potential to differentiate and contribute to multiple tumor properties, such as recurrence, metastasis, heterogeneity, multidrug resistance, and radiation resistance. Thus, CSCs are considered to be promising therapeutic targets for cancer therapy. The function of CSCs can be regulated by ubiquitination and deubiquitination of proteins related to the specific stemness of the cells executing various stem cell fate choices. To regulate the balance between ubiquitination and deubiquitination processes, the disassembly of ubiquitin chains from specific substrates by deubiquitinating enzymes (DUBs) is crucial. Several key developmental and signaling pathways have been shown to play essential roles in this regulation. Growing evidence suggests that overactive or abnormal signaling within and among these pathways may contribute to the survival of CSCs. These signaling pathways have been experimentally shown to mediate various stem cell properties, such as self-renewal, cell fate decisions, survival, proliferation, and differentiation. In this review, we focus on the DUBs involved in CSCs signaling pathways, which are vital in regulating their stem-cell fate determination. MDPI 2020-11-04 /pmc/articles/PMC7694198/ /pubmed/33158118 http://dx.doi.org/10.3390/cancers12113253 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Kaushal, Kamini Ramakrishna, Suresh Deubiquitinating Enzyme-Mediated Signaling Networks in Cancer Stem Cells |
title | Deubiquitinating Enzyme-Mediated Signaling Networks in Cancer Stem Cells |
title_full | Deubiquitinating Enzyme-Mediated Signaling Networks in Cancer Stem Cells |
title_fullStr | Deubiquitinating Enzyme-Mediated Signaling Networks in Cancer Stem Cells |
title_full_unstemmed | Deubiquitinating Enzyme-Mediated Signaling Networks in Cancer Stem Cells |
title_short | Deubiquitinating Enzyme-Mediated Signaling Networks in Cancer Stem Cells |
title_sort | deubiquitinating enzyme-mediated signaling networks in cancer stem cells |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7694198/ https://www.ncbi.nlm.nih.gov/pubmed/33158118 http://dx.doi.org/10.3390/cancers12113253 |
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