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CK2α通过PI3K/Akt/GSK-3β信号通路调控肺腺癌A549细胞的侵袭及迁移
BACKGROUND AND OBJECTIVE: Lung cancer is the leading cancer-related death worldwide. Patients with lung cancer mainly died of tumor metastasis and invasion. Protein kinase CK2 is an ubiquitous serine/threonine protein kinase and is frequently upregulated in various human tumors. This study aims to e...
Formato: | Online Artículo Texto |
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Lenguaje: | English |
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中国肺癌杂志编辑部
2017
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5999677/ https://www.ncbi.nlm.nih.gov/pubmed/28442011 http://dx.doi.org/10.3779/j.issn.1009-3419.2017.04.11 |
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collection | PubMed |
description | BACKGROUND AND OBJECTIVE: Lung cancer is the leading cancer-related death worldwide. Patients with lung cancer mainly died of tumor metastasis and invasion. Protein kinase CK2 is an ubiquitous serine/threonine protein kinase and is frequently upregulated in various human tumors. This study aims to explore the effect and molecular mechanism of the invasion and migration of lung adenocarcinoma A549 cells after knock-down of CK2α expression. METHODS: The pSilencer(TM) 4.1-siCK2α-eGFP of lentiviral-mediated shRNA was constructed. The expression of CK2α was knock-downed, and a stable A549 cell line was established. The invasion and migration of A549 cell line was detected through Transwell and Boyden chamber assays. The protein expression of the PI3K/Akt signaling pathway and mesenchymal-to-epithelial transition (EMT) was evaluated using Western blot analysis. RESULTS: The invasion and migration of A549 cells were significantly inhibited after the knockdown of CK2α expression compared with that in the control group. p-PTEN, Akt, p-Akt(473), p-Akt(308), p-PDK1, p-c-Raf, and p-GSK-3β were significantly downregulated, whereas PTEN was upregulated. Moreover, vimentin, β-catenin, Snail, MMP2, and MMP9 were significantly downregulated after reducing the CK2α expression. CONCLUSION: CK2α might regulate the invasion and migration of A549 cells through the PI3K/Akt/GSK-3β/Snail signaling pathway, which controls EMT in lung adenocarcinoma. |
format | Online Article Text |
id | pubmed-5999677 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | 中国肺癌杂志编辑部 |
record_format | MEDLINE/PubMed |
spelling | pubmed-59996772018-07-06 CK2α通过PI3K/Akt/GSK-3β信号通路调控肺腺癌A549细胞的侵袭及迁移 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: Lung cancer is the leading cancer-related death worldwide. Patients with lung cancer mainly died of tumor metastasis and invasion. Protein kinase CK2 is an ubiquitous serine/threonine protein kinase and is frequently upregulated in various human tumors. This study aims to explore the effect and molecular mechanism of the invasion and migration of lung adenocarcinoma A549 cells after knock-down of CK2α expression. METHODS: The pSilencer(TM) 4.1-siCK2α-eGFP of lentiviral-mediated shRNA was constructed. The expression of CK2α was knock-downed, and a stable A549 cell line was established. The invasion and migration of A549 cell line was detected through Transwell and Boyden chamber assays. The protein expression of the PI3K/Akt signaling pathway and mesenchymal-to-epithelial transition (EMT) was evaluated using Western blot analysis. RESULTS: The invasion and migration of A549 cells were significantly inhibited after the knockdown of CK2α expression compared with that in the control group. p-PTEN, Akt, p-Akt(473), p-Akt(308), p-PDK1, p-c-Raf, and p-GSK-3β were significantly downregulated, whereas PTEN was upregulated. Moreover, vimentin, β-catenin, Snail, MMP2, and MMP9 were significantly downregulated after reducing the CK2α expression. CONCLUSION: CK2α might regulate the invasion and migration of A549 cells through the PI3K/Akt/GSK-3β/Snail signaling pathway, which controls EMT in lung adenocarcinoma. 中国肺癌杂志编辑部 2017-04-20 /pmc/articles/PMC5999677/ /pubmed/28442011 http://dx.doi.org/10.3779/j.issn.1009-3419.2017.04.11 Text en 版权所有©《中国肺癌杂志》编辑部2017 https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/ |
spellingShingle | 基础研究 CK2α通过PI3K/Akt/GSK-3β信号通路调控肺腺癌A549细胞的侵袭及迁移 |
title | CK2α通过PI3K/Akt/GSK-3β信号通路调控肺腺癌A549细胞的侵袭及迁移 |
title_full | CK2α通过PI3K/Akt/GSK-3β信号通路调控肺腺癌A549细胞的侵袭及迁移 |
title_fullStr | CK2α通过PI3K/Akt/GSK-3β信号通路调控肺腺癌A549细胞的侵袭及迁移 |
title_full_unstemmed | CK2α通过PI3K/Akt/GSK-3β信号通路调控肺腺癌A549细胞的侵袭及迁移 |
title_short | CK2α通过PI3K/Akt/GSK-3β信号通路调控肺腺癌A549细胞的侵袭及迁移 |
title_sort | ck2α通过pi3k/akt/gsk-3β信号通路调控肺腺癌a549细胞的侵袭及迁移 |
topic | 基础研究 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5999677/ https://www.ncbi.nlm.nih.gov/pubmed/28442011 http://dx.doi.org/10.3779/j.issn.1009-3419.2017.04.11 |
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