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Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy
Lung cancer is a leading cause of global cancer deaths. Na/K-ATPase has been studied as a target for cancer treatment. Cardiotonic steroids (CS) trigger intracellular signalling upon binding to Na/K-ATPase. Normal lung and tumour cells frequently express different pump isoforms. Thus, Na/K-ATPase is...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6154632/ https://www.ncbi.nlm.nih.gov/pubmed/28430151 http://dx.doi.org/10.3390/molecules22040578 |
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author | Felippe Gonçalves-de-Albuquerque, Cassiano Ribeiro Silva, Adriana Ignácio da Silva, Camila Caire Castro-Faria-Neto, Hugo Burth, Patrícia |
author_facet | Felippe Gonçalves-de-Albuquerque, Cassiano Ribeiro Silva, Adriana Ignácio da Silva, Camila Caire Castro-Faria-Neto, Hugo Burth, Patrícia |
author_sort | Felippe Gonçalves-de-Albuquerque, Cassiano |
collection | PubMed |
description | Lung cancer is a leading cause of global cancer deaths. Na/K-ATPase has been studied as a target for cancer treatment. Cardiotonic steroids (CS) trigger intracellular signalling upon binding to Na/K-ATPase. Normal lung and tumour cells frequently express different pump isoforms. Thus, Na/K-ATPase is a powerful target for lung cancer treatment. Drugs targeting Na/K-ATPase may induce apoptosis and autophagy in transformed cells. We argue that Na/K-ATPase has a role as a potential target in chemotherapy in lung cancer treatment. We discuss the effects of Na/K-ATPase ligands and molecular pathways inducing deleterious effects on lung cancer cells, especially those leading to apoptosis and autophagy. |
format | Online Article Text |
id | pubmed-6154632 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-61546322018-11-13 Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy Felippe Gonçalves-de-Albuquerque, Cassiano Ribeiro Silva, Adriana Ignácio da Silva, Camila Caire Castro-Faria-Neto, Hugo Burth, Patrícia Molecules Review Lung cancer is a leading cause of global cancer deaths. Na/K-ATPase has been studied as a target for cancer treatment. Cardiotonic steroids (CS) trigger intracellular signalling upon binding to Na/K-ATPase. Normal lung and tumour cells frequently express different pump isoforms. Thus, Na/K-ATPase is a powerful target for lung cancer treatment. Drugs targeting Na/K-ATPase may induce apoptosis and autophagy in transformed cells. We argue that Na/K-ATPase has a role as a potential target in chemotherapy in lung cancer treatment. We discuss the effects of Na/K-ATPase ligands and molecular pathways inducing deleterious effects on lung cancer cells, especially those leading to apoptosis and autophagy. MDPI 2017-04-21 /pmc/articles/PMC6154632/ /pubmed/28430151 http://dx.doi.org/10.3390/molecules22040578 Text en © 2017 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 Felippe Gonçalves-de-Albuquerque, Cassiano Ribeiro Silva, Adriana Ignácio da Silva, Camila Caire Castro-Faria-Neto, Hugo Burth, Patrícia Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy |
title | Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy |
title_full | Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy |
title_fullStr | Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy |
title_full_unstemmed | Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy |
title_short | Na/K Pump and Beyond: Na/K-ATPase as a Modulator of Apoptosis and Autophagy |
title_sort | na/k pump and beyond: na/k-atpase as a modulator of apoptosis and autophagy |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6154632/ https://www.ncbi.nlm.nih.gov/pubmed/28430151 http://dx.doi.org/10.3390/molecules22040578 |
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