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Targeting calcium signaling in cancer therapy

The intracellular calcium ions (Ca(2+)) act as second messenger to regulate gene transcription, cell proliferation, migration and death. Accumulating evidences have demonstrated that intracellular Ca(2+) homeostasis is altered in cancer cells and the alteration is involved in tumor initiation, angio...

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Detalles Bibliográficos
Autores principales: Cui, Chaochu, Merritt, Robert, Fu, Liwu, Pan, Zui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5237760/
https://www.ncbi.nlm.nih.gov/pubmed/28119804
http://dx.doi.org/10.1016/j.apsb.2016.11.001
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author Cui, Chaochu
Merritt, Robert
Fu, Liwu
Pan, Zui
author_facet Cui, Chaochu
Merritt, Robert
Fu, Liwu
Pan, Zui
author_sort Cui, Chaochu
collection PubMed
description The intracellular calcium ions (Ca(2+)) act as second messenger to regulate gene transcription, cell proliferation, migration and death. Accumulating evidences have demonstrated that intracellular Ca(2+) homeostasis is altered in cancer cells and the alteration is involved in tumor initiation, angiogenesis, progression and metastasis. Targeting derailed Ca(2+) signaling for cancer therapy has become an emerging research area. This review summarizes some important Ca(2+) channels, transporters and Ca(2+)-ATPases, which have been reported to be altered in human cancer patients. It discusses the current research effort toward evaluation of the blockers, inhibitors or regulators for Ca(2+) channels/transporters or Ca(2+)-ATPase pumps as anti-cancer drugs. This review is also aimed to stimulate interest in, and support for research into the understanding of cellular mechanisms underlying the regulation of Ca(2+) signaling in different cancer cells, and to search for novel therapies to cure these malignancies by targeting Ca(2+) channels or transporters.
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spelling pubmed-52377602017-01-24 Targeting calcium signaling in cancer therapy Cui, Chaochu Merritt, Robert Fu, Liwu Pan, Zui Acta Pharm Sin B Review The intracellular calcium ions (Ca(2+)) act as second messenger to regulate gene transcription, cell proliferation, migration and death. Accumulating evidences have demonstrated that intracellular Ca(2+) homeostasis is altered in cancer cells and the alteration is involved in tumor initiation, angiogenesis, progression and metastasis. Targeting derailed Ca(2+) signaling for cancer therapy has become an emerging research area. This review summarizes some important Ca(2+) channels, transporters and Ca(2+)-ATPases, which have been reported to be altered in human cancer patients. It discusses the current research effort toward evaluation of the blockers, inhibitors or regulators for Ca(2+) channels/transporters or Ca(2+)-ATPase pumps as anti-cancer drugs. This review is also aimed to stimulate interest in, and support for research into the understanding of cellular mechanisms underlying the regulation of Ca(2+) signaling in different cancer cells, and to search for novel therapies to cure these malignancies by targeting Ca(2+) channels or transporters. Elsevier 2017-01 2016-12-13 /pmc/articles/PMC5237760/ /pubmed/28119804 http://dx.doi.org/10.1016/j.apsb.2016.11.001 Text en © 2017 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review
Cui, Chaochu
Merritt, Robert
Fu, Liwu
Pan, Zui
Targeting calcium signaling in cancer therapy
title Targeting calcium signaling in cancer therapy
title_full Targeting calcium signaling in cancer therapy
title_fullStr Targeting calcium signaling in cancer therapy
title_full_unstemmed Targeting calcium signaling in cancer therapy
title_short Targeting calcium signaling in cancer therapy
title_sort targeting calcium signaling in cancer therapy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5237760/
https://www.ncbi.nlm.nih.gov/pubmed/28119804
http://dx.doi.org/10.1016/j.apsb.2016.11.001
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