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Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability

Potassium voltage-gated channel subfamily A member 5 (KCNA5) is a voltage-gated potassium channel protein encoded by the KCNA5 gene. A large number of studies have shown that KCNA5 is associated with the survival of malignant tumors, including breast cancer, but the detailed mechanism remains inconc...

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Autores principales: Qu, Chao, Sun, Jia, Liu, Ying, Wang, Xiaobo, Wang, Lifen, Han, Chao, Chen, Qian, Guan, Tianhui, Li, Hongyan, Zhang, Yejun, Wang, Yang, Liu, Jia, Zou, Wei, Liu, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6144920/
https://www.ncbi.nlm.nih.gov/pubmed/30250548
http://dx.doi.org/10.3892/ol.2018.9261
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author Qu, Chao
Sun, Jia
Liu, Ying
Wang, Xiaobo
Wang, Lifen
Han, Chao
Chen, Qian
Guan, Tianhui
Li, Hongyan
Zhang, Yejun
Wang, Yang
Liu, Jia
Zou, Wei
Liu, Jing
author_facet Qu, Chao
Sun, Jia
Liu, Ying
Wang, Xiaobo
Wang, Lifen
Han, Chao
Chen, Qian
Guan, Tianhui
Li, Hongyan
Zhang, Yejun
Wang, Yang
Liu, Jia
Zou, Wei
Liu, Jing
author_sort Qu, Chao
collection PubMed
description Potassium voltage-gated channel subfamily A member 5 (KCNA5) is a voltage-gated potassium channel protein encoded by the KCNA5 gene. A large number of studies have shown that KCNA5 is associated with the survival of malignant tumors, including breast cancer, but the detailed mechanism remains inconclusive. Our previous study found that KCNA5 is co-expressed with a scaffolding protein, caveolin-1 in MCF-10A-neoT non-tumorigenic epithelial cell. In the present study, KCNA5 and caveolin-1 were expressed in breast cancer tissues and cell lines. Exposing MCF-10A-neoT to 2 mM of methyl-β-cyclodextrin, an agent to disrupt caveolae and lipid rafts led to a downregulation of caveolin-1 that reduced the expression of KCNA5. Furthermore, following caveolin-1 knockdown, the expression of KCNA5 was decreased in MDA-MB-231 human breast cancer and MCF-10A-neoT non-tumorigenic epithelial cell lines. In subsequent experiments, the MTT assay showed that increased caveolin-1 and KCNA5 expression promoted the survival of MCF-7 human breast cancer cells, but cell survival was not affected following KCNA5 overexpression alone. Using small interfering RNA technology, KCNA5-silenced MCF-10A-neoT cells were established and a decreased level of phosphorylated-AKT serine/threonine kinase (AKT) was observed in the cells compared with the parental cells. Overall, these results suggested that caveolin-1 facilitated KCNA5 expression and may be associated with AKT activation.
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spelling pubmed-61449202018-09-24 Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability Qu, Chao Sun, Jia Liu, Ying Wang, Xiaobo Wang, Lifen Han, Chao Chen, Qian Guan, Tianhui Li, Hongyan Zhang, Yejun Wang, Yang Liu, Jia Zou, Wei Liu, Jing Oncol Lett Articles Potassium voltage-gated channel subfamily A member 5 (KCNA5) is a voltage-gated potassium channel protein encoded by the KCNA5 gene. A large number of studies have shown that KCNA5 is associated with the survival of malignant tumors, including breast cancer, but the detailed mechanism remains inconclusive. Our previous study found that KCNA5 is co-expressed with a scaffolding protein, caveolin-1 in MCF-10A-neoT non-tumorigenic epithelial cell. In the present study, KCNA5 and caveolin-1 were expressed in breast cancer tissues and cell lines. Exposing MCF-10A-neoT to 2 mM of methyl-β-cyclodextrin, an agent to disrupt caveolae and lipid rafts led to a downregulation of caveolin-1 that reduced the expression of KCNA5. Furthermore, following caveolin-1 knockdown, the expression of KCNA5 was decreased in MDA-MB-231 human breast cancer and MCF-10A-neoT non-tumorigenic epithelial cell lines. In subsequent experiments, the MTT assay showed that increased caveolin-1 and KCNA5 expression promoted the survival of MCF-7 human breast cancer cells, but cell survival was not affected following KCNA5 overexpression alone. Using small interfering RNA technology, KCNA5-silenced MCF-10A-neoT cells were established and a decreased level of phosphorylated-AKT serine/threonine kinase (AKT) was observed in the cells compared with the parental cells. Overall, these results suggested that caveolin-1 facilitated KCNA5 expression and may be associated with AKT activation. D.A. Spandidos 2018-10 2018-08-03 /pmc/articles/PMC6144920/ /pubmed/30250548 http://dx.doi.org/10.3892/ol.2018.9261 Text en Copyright: © Qu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Qu, Chao
Sun, Jia
Liu, Ying
Wang, Xiaobo
Wang, Lifen
Han, Chao
Chen, Qian
Guan, Tianhui
Li, Hongyan
Zhang, Yejun
Wang, Yang
Liu, Jia
Zou, Wei
Liu, Jing
Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability
title Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability
title_full Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability
title_fullStr Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability
title_full_unstemmed Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability
title_short Caveolin-1 facilitated KCNA5 expression, promoting breast cancer viability
title_sort caveolin-1 facilitated kcna5 expression, promoting breast cancer viability
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6144920/
https://www.ncbi.nlm.nih.gov/pubmed/30250548
http://dx.doi.org/10.3892/ol.2018.9261
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