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IL-23促进人肺腺癌A549细胞的迁移和侵袭
BACKGROUND AND OBJECTIVE: Interleukin 23 (IL-23) is a pro-inflammatory cytokine that plays an important role in inflammatory disease and tumor microenvironment. The IL-23 receptor is expressed in colon, lung, and oral carcinomas. We performed this study to investigate whether IL-23 promotes directly...
Formato: | Online Artículo Texto |
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Lenguaje: | English |
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中国肺癌杂志编辑部
2012
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000124/ https://www.ncbi.nlm.nih.gov/pubmed/22613329 http://dx.doi.org/10.3779/j.issn.1009-3419.2012.05.01 |
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collection | PubMed |
description | BACKGROUND AND OBJECTIVE: Interleukin 23 (IL-23) is a pro-inflammatory cytokine that plays an important role in inflammatory disease and tumor microenvironment. The IL-23 receptor is expressed in colon, lung, and oral carcinomas. We performed this study to investigate whether IL-23 promotes directly carcinoma cell migration and invasion as well as further explore its mechanism. METHODS: The migration and invasion of human lung adenocarcinoma A549 cells induced by IL-23 were detected by a scratch test and Transwell experiment. MMP-9 expression of the mRNA and protein levels of A549 cells cultured with and without IL-23 was respectively detected by Real-time PCR and ELISA. The effect of IL-23 on A549 cells was further verified using anti-IL-23p19 neutralization antibody (Ab IL-23p19) to eliminate IL-23. RESULTS: IL-23 remarkably promoted A549 cell migration and invasion. MMP-9 expression in A549 cells was upregulated by IL-23 stimulation. In addition, the effect of IL-23 on the migration and invasion of A549, as well as the MMP-9 expression in A549 cells induced by IL-23, was eliminated by Ab IL-23p19. CONCLUSION: IL-23 promotes the migration and invasion of A549 cells by inducing MMP-9 expression. |
format | Online Article Text |
id | pubmed-6000124 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | 中国肺癌杂志编辑部 |
record_format | MEDLINE/PubMed |
spelling | pubmed-60001242018-07-06 IL-23促进人肺腺癌A549细胞的迁移和侵袭 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: Interleukin 23 (IL-23) is a pro-inflammatory cytokine that plays an important role in inflammatory disease and tumor microenvironment. The IL-23 receptor is expressed in colon, lung, and oral carcinomas. We performed this study to investigate whether IL-23 promotes directly carcinoma cell migration and invasion as well as further explore its mechanism. METHODS: The migration and invasion of human lung adenocarcinoma A549 cells induced by IL-23 were detected by a scratch test and Transwell experiment. MMP-9 expression of the mRNA and protein levels of A549 cells cultured with and without IL-23 was respectively detected by Real-time PCR and ELISA. The effect of IL-23 on A549 cells was further verified using anti-IL-23p19 neutralization antibody (Ab IL-23p19) to eliminate IL-23. RESULTS: IL-23 remarkably promoted A549 cell migration and invasion. MMP-9 expression in A549 cells was upregulated by IL-23 stimulation. In addition, the effect of IL-23 on the migration and invasion of A549, as well as the MMP-9 expression in A549 cells induced by IL-23, was eliminated by Ab IL-23p19. CONCLUSION: IL-23 promotes the migration and invasion of A549 cells by inducing MMP-9 expression. 中国肺癌杂志编辑部 2012-05-20 /pmc/articles/PMC6000124/ /pubmed/22613329 http://dx.doi.org/10.3779/j.issn.1009-3419.2012.05.01 Text en 版权所有©《中国肺癌杂志》编辑部2012 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 IL-23促进人肺腺癌A549细胞的迁移和侵袭 |
title | IL-23促进人肺腺癌A549细胞的迁移和侵袭 |
title_full | IL-23促进人肺腺癌A549细胞的迁移和侵袭 |
title_fullStr | IL-23促进人肺腺癌A549细胞的迁移和侵袭 |
title_full_unstemmed | IL-23促进人肺腺癌A549细胞的迁移和侵袭 |
title_short | IL-23促进人肺腺癌A549细胞的迁移和侵袭 |
title_sort | il-23促进人肺腺癌a549细胞的迁移和侵袭 |
topic | 基础研究 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000124/ https://www.ncbi.nlm.nih.gov/pubmed/22613329 http://dx.doi.org/10.3779/j.issn.1009-3419.2012.05.01 |
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