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Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage
Voltage-gated potassium channel subfamily A member 1 (KCNA1/Kv1.1) is an important component of type A potassium channels, which has been found to be involved in various tumors. This study aimed to identify the role of KCNA1 in cervical cancer and explore the related mechanism. The levels of KCNA1 i...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6682364/ https://www.ncbi.nlm.nih.gov/pubmed/31354026 http://dx.doi.org/10.1080/19336950.2019.1648627 |
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author | Liu, Li Chen, Yumei Zhang, Qingyuan Li, Changzhong |
author_facet | Liu, Li Chen, Yumei Zhang, Qingyuan Li, Changzhong |
author_sort | Liu, Li |
collection | PubMed |
description | Voltage-gated potassium channel subfamily A member 1 (KCNA1/Kv1.1) is an important component of type A potassium channels, which has been found to be involved in various tumors. This study aimed to identify the role of KCNA1 in cervical cancer and explore the related mechanism. The levels of KCNA1 in cervical cancer tissues and cell lines were examined by Western blot and qPCR. Cell proliferation and invasion were assessed by CCK-8 and transwell assays, respectively. Protein levels of Hedgehog (Hhg), Wnt and Notch were detected by Western blot. The mitochondrial capacity was examined by immunostaining with MitoTracker Red CMXRos. KCNA1 was highly expressed in cervical cancer tissues and cell lines, and correlated with poor prognosis. In addition, depletion of KCNA1 suppressed growth, proliferation, migration and invasion of HeLa cells. Moreover, KCNA1 could regulate the Hhg, Wnt and Notch signaling pathways and cause mitochondrial dysfunction. The present study has demonstrated that KCNA1 is an oncogene excessively expressed in cervical cancer, and promotes tumor progression by regulating the Hhg, Wnt and Notch signaling pathways and the mitochondrial capacity. Therefore, our results provide a theoretical basis for the discovery of novel clinical treatment against cervical cancer. |
format | Online Article Text |
id | pubmed-6682364 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-66823642019-08-14 Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage Liu, Li Chen, Yumei Zhang, Qingyuan Li, Changzhong Channels (Austin) Research Paper Voltage-gated potassium channel subfamily A member 1 (KCNA1/Kv1.1) is an important component of type A potassium channels, which has been found to be involved in various tumors. This study aimed to identify the role of KCNA1 in cervical cancer and explore the related mechanism. The levels of KCNA1 in cervical cancer tissues and cell lines were examined by Western blot and qPCR. Cell proliferation and invasion were assessed by CCK-8 and transwell assays, respectively. Protein levels of Hedgehog (Hhg), Wnt and Notch were detected by Western blot. The mitochondrial capacity was examined by immunostaining with MitoTracker Red CMXRos. KCNA1 was highly expressed in cervical cancer tissues and cell lines, and correlated with poor prognosis. In addition, depletion of KCNA1 suppressed growth, proliferation, migration and invasion of HeLa cells. Moreover, KCNA1 could regulate the Hhg, Wnt and Notch signaling pathways and cause mitochondrial dysfunction. The present study has demonstrated that KCNA1 is an oncogene excessively expressed in cervical cancer, and promotes tumor progression by regulating the Hhg, Wnt and Notch signaling pathways and the mitochondrial capacity. Therefore, our results provide a theoretical basis for the discovery of novel clinical treatment against cervical cancer. Taylor & Francis 2019-07-27 /pmc/articles/PMC6682364/ /pubmed/31354026 http://dx.doi.org/10.1080/19336950.2019.1648627 Text en © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Paper Liu, Li Chen, Yumei Zhang, Qingyuan Li, Changzhong Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage |
title | Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage |
title_full | Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage |
title_fullStr | Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage |
title_full_unstemmed | Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage |
title_short | Silencing of KCNA1 suppresses the cervical cancer development via mitochondria damage |
title_sort | silencing of kcna1 suppresses the cervical cancer development via mitochondria damage |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6682364/ https://www.ncbi.nlm.nih.gov/pubmed/31354026 http://dx.doi.org/10.1080/19336950.2019.1648627 |
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