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Role of Calcium Homeostasis in Modulating EMT in Cancer

Calcium is essential for cells to perform numerous physiological processes. In cancer, the augmentation of calcium signaling supports the more proliferative and migratory cells, which is a characteristic of the epithelial-to-mesenchymal transition (EMT). By genetically and epigenetically modifying g...

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Detalles Bibliográficos
Autores principales: Jones, Clark A., Hazlehurst, Lori A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8471317/
https://www.ncbi.nlm.nih.gov/pubmed/34572386
http://dx.doi.org/10.3390/biomedicines9091200
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author Jones, Clark A.
Hazlehurst, Lori A.
author_facet Jones, Clark A.
Hazlehurst, Lori A.
author_sort Jones, Clark A.
collection PubMed
description Calcium is essential for cells to perform numerous physiological processes. In cancer, the augmentation of calcium signaling supports the more proliferative and migratory cells, which is a characteristic of the epithelial-to-mesenchymal transition (EMT). By genetically and epigenetically modifying genes, channels, and entire signaling pathways, cancer cells have adapted to survive with an extreme imbalance of calcium that allows them to grow and metastasize in an abnormal manner. This cellular remodeling also allows for the evasion of immune surveillance and the development of drug resistance, which lead to poor prognosis in patients. Understanding the role calcium flux plays in driving the phenotypes associated with invasion, immune suppression, metastasis, and drug resistance remains critical for determining treatments to optimize clinical outcomes and future drug discovery.
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spelling pubmed-84713172021-09-27 Role of Calcium Homeostasis in Modulating EMT in Cancer Jones, Clark A. Hazlehurst, Lori A. Biomedicines Review Calcium is essential for cells to perform numerous physiological processes. In cancer, the augmentation of calcium signaling supports the more proliferative and migratory cells, which is a characteristic of the epithelial-to-mesenchymal transition (EMT). By genetically and epigenetically modifying genes, channels, and entire signaling pathways, cancer cells have adapted to survive with an extreme imbalance of calcium that allows them to grow and metastasize in an abnormal manner. This cellular remodeling also allows for the evasion of immune surveillance and the development of drug resistance, which lead to poor prognosis in patients. Understanding the role calcium flux plays in driving the phenotypes associated with invasion, immune suppression, metastasis, and drug resistance remains critical for determining treatments to optimize clinical outcomes and future drug discovery. MDPI 2021-09-11 /pmc/articles/PMC8471317/ /pubmed/34572386 http://dx.doi.org/10.3390/biomedicines9091200 Text en © 2021 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
Jones, Clark A.
Hazlehurst, Lori A.
Role of Calcium Homeostasis in Modulating EMT in Cancer
title Role of Calcium Homeostasis in Modulating EMT in Cancer
title_full Role of Calcium Homeostasis in Modulating EMT in Cancer
title_fullStr Role of Calcium Homeostasis in Modulating EMT in Cancer
title_full_unstemmed Role of Calcium Homeostasis in Modulating EMT in Cancer
title_short Role of Calcium Homeostasis in Modulating EMT in Cancer
title_sort role of calcium homeostasis in modulating emt in cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8471317/
https://www.ncbi.nlm.nih.gov/pubmed/34572386
http://dx.doi.org/10.3390/biomedicines9091200
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