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Association of protein kinase CK2 inhibition with cellular radiosensitivity of non-small cell lung cancer
Protein kinase CK2 is a highly conserved protein Ser/Thr protein kinase and plays important roles in cell proliferation, protein translation and cell survival. This study investigated the possibility of using CK2 inhibition as a new approach for increasing the efficacy of radiotherapy in non-small c...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5700935/ https://www.ncbi.nlm.nih.gov/pubmed/29170453 http://dx.doi.org/10.1038/s41598-017-16012-1 |
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author | Li, Qianwen Li, Ke Yang, Tianyang Zhang, Sheng Zhou, Yu Li, Zhenyu Xiong, Jinrong Zhou, Fangzheng Zhou, Xiaoshu Liu, Li Meng, Rui Wu, Gang |
author_facet | Li, Qianwen Li, Ke Yang, Tianyang Zhang, Sheng Zhou, Yu Li, Zhenyu Xiong, Jinrong Zhou, Fangzheng Zhou, Xiaoshu Liu, Li Meng, Rui Wu, Gang |
author_sort | Li, Qianwen |
collection | PubMed |
description | Protein kinase CK2 is a highly conserved protein Ser/Thr protein kinase and plays important roles in cell proliferation, protein translation and cell survival. This study investigated the possibility of using CK2 inhibition as a new approach for increasing the efficacy of radiotherapy in non-small cell lung cancer (NSCLC) and its underlying mechanisms. Kinase inhibition of CK2 was attempted either by using the specific CK2 inhibitor, Quinalizarin or by applying siRNA interference technology to silence the expression of the catalytic subunit of CK2 in A549 and H460 cells. The results showed that CK2α knockdown or Quinalizarin significantly enhanced the radiosensitivity of various NSCLC cells. The notable findings we observed after exposure to both CK2 inhibition and ionizing radiation (IR) were a prolonged delay in radiation-induced DNA double-strand breaks (DSB) repair, robust G2/M checkpoint arrest and increased apoptosis. In vivo studies further demonstrated that compared with each treatment alone, CK2 inhibition combined with IR reduced tumor growth in the H460 cell xenograft model. In conclusion, CK2 is a promising target for the enhancement of radiosensitivity in NSCLC. |
format | Online Article Text |
id | pubmed-5700935 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57009352017-11-30 Association of protein kinase CK2 inhibition with cellular radiosensitivity of non-small cell lung cancer Li, Qianwen Li, Ke Yang, Tianyang Zhang, Sheng Zhou, Yu Li, Zhenyu Xiong, Jinrong Zhou, Fangzheng Zhou, Xiaoshu Liu, Li Meng, Rui Wu, Gang Sci Rep Article Protein kinase CK2 is a highly conserved protein Ser/Thr protein kinase and plays important roles in cell proliferation, protein translation and cell survival. This study investigated the possibility of using CK2 inhibition as a new approach for increasing the efficacy of radiotherapy in non-small cell lung cancer (NSCLC) and its underlying mechanisms. Kinase inhibition of CK2 was attempted either by using the specific CK2 inhibitor, Quinalizarin or by applying siRNA interference technology to silence the expression of the catalytic subunit of CK2 in A549 and H460 cells. The results showed that CK2α knockdown or Quinalizarin significantly enhanced the radiosensitivity of various NSCLC cells. The notable findings we observed after exposure to both CK2 inhibition and ionizing radiation (IR) were a prolonged delay in radiation-induced DNA double-strand breaks (DSB) repair, robust G2/M checkpoint arrest and increased apoptosis. In vivo studies further demonstrated that compared with each treatment alone, CK2 inhibition combined with IR reduced tumor growth in the H460 cell xenograft model. In conclusion, CK2 is a promising target for the enhancement of radiosensitivity in NSCLC. Nature Publishing Group UK 2017-11-23 /pmc/articles/PMC5700935/ /pubmed/29170453 http://dx.doi.org/10.1038/s41598-017-16012-1 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Li, Qianwen Li, Ke Yang, Tianyang Zhang, Sheng Zhou, Yu Li, Zhenyu Xiong, Jinrong Zhou, Fangzheng Zhou, Xiaoshu Liu, Li Meng, Rui Wu, Gang Association of protein kinase CK2 inhibition with cellular radiosensitivity of non-small cell lung cancer |
title | Association of protein kinase CK2 inhibition with cellular radiosensitivity of non-small cell lung cancer |
title_full | Association of protein kinase CK2 inhibition with cellular radiosensitivity of non-small cell lung cancer |
title_fullStr | Association of protein kinase CK2 inhibition with cellular radiosensitivity of non-small cell lung cancer |
title_full_unstemmed | Association of protein kinase CK2 inhibition with cellular radiosensitivity of non-small cell lung cancer |
title_short | Association of protein kinase CK2 inhibition with cellular radiosensitivity of non-small cell lung cancer |
title_sort | association of protein kinase ck2 inhibition with cellular radiosensitivity of non-small cell lung cancer |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5700935/ https://www.ncbi.nlm.nih.gov/pubmed/29170453 http://dx.doi.org/10.1038/s41598-017-16012-1 |
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