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Potential to Eradicate Cancer Stemness by Targeting Cell Surface GRP78
Cancer stemness is proposed to be the main cause of metastasis and tumor relapse after conventional therapy due to the main properties of cancer stem cells. These include unlimited self-renewal, the low percentage in a cell population, asymmetric/symmetric cell division, and the hypothetical differe...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9313351/ https://www.ncbi.nlm.nih.gov/pubmed/35883497 http://dx.doi.org/10.3390/biom12070941 |
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author | Chen, Hsin-Ying Cheng, Ann-Joy |
author_facet | Chen, Hsin-Ying Cheng, Ann-Joy |
author_sort | Chen, Hsin-Ying |
collection | PubMed |
description | Cancer stemness is proposed to be the main cause of metastasis and tumor relapse after conventional therapy due to the main properties of cancer stem cells. These include unlimited self-renewal, the low percentage in a cell population, asymmetric/symmetric cell division, and the hypothetical different nature for absorbing external substances. As the mechanism of how cancer stemness is maintained remains unknown, further investigation into the basic features of cancer stemness is required. Many articles demonstrated that glucose-regulated protein 78 (GRP78) plays a key role in cancer stemness, suggesting that this molecule is feasible for targeting cancer stem cells. This review summarizes the history of finding cancer stem cells, as well as the functions of GRP78 in cancer stemness, for discussing the possibility of targeting GRP78 to eradicate cancer stemness. |
format | Online Article Text |
id | pubmed-9313351 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-93133512022-07-26 Potential to Eradicate Cancer Stemness by Targeting Cell Surface GRP78 Chen, Hsin-Ying Cheng, Ann-Joy Biomolecules Review Cancer stemness is proposed to be the main cause of metastasis and tumor relapse after conventional therapy due to the main properties of cancer stem cells. These include unlimited self-renewal, the low percentage in a cell population, asymmetric/symmetric cell division, and the hypothetical different nature for absorbing external substances. As the mechanism of how cancer stemness is maintained remains unknown, further investigation into the basic features of cancer stemness is required. Many articles demonstrated that glucose-regulated protein 78 (GRP78) plays a key role in cancer stemness, suggesting that this molecule is feasible for targeting cancer stem cells. This review summarizes the history of finding cancer stem cells, as well as the functions of GRP78 in cancer stemness, for discussing the possibility of targeting GRP78 to eradicate cancer stemness. MDPI 2022-07-05 /pmc/articles/PMC9313351/ /pubmed/35883497 http://dx.doi.org/10.3390/biom12070941 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Chen, Hsin-Ying Cheng, Ann-Joy Potential to Eradicate Cancer Stemness by Targeting Cell Surface GRP78 |
title | Potential to Eradicate Cancer Stemness by Targeting Cell Surface GRP78 |
title_full | Potential to Eradicate Cancer Stemness by Targeting Cell Surface GRP78 |
title_fullStr | Potential to Eradicate Cancer Stemness by Targeting Cell Surface GRP78 |
title_full_unstemmed | Potential to Eradicate Cancer Stemness by Targeting Cell Surface GRP78 |
title_short | Potential to Eradicate Cancer Stemness by Targeting Cell Surface GRP78 |
title_sort | potential to eradicate cancer stemness by targeting cell surface grp78 |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9313351/ https://www.ncbi.nlm.nih.gov/pubmed/35883497 http://dx.doi.org/10.3390/biom12070941 |
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