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IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition
The characteristics of cancer cells, such as invasiveness, are affected by the tumor microenvironment. Studies have shown that interleukin (IL)-6 and tumor necrosis factor (TNF)-α regulate the proliferation of lung cancer. However, few studies have focused on the effects of IL-6 and TNF-α on metasta...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452994/ https://www.ncbi.nlm.nih.gov/pubmed/28599466 http://dx.doi.org/10.3892/ol.2017.6048 |
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author | Shang, Guan-Sheng Liu, Lunxu Qin, Yi-Wei |
author_facet | Shang, Guan-Sheng Liu, Lunxu Qin, Yi-Wei |
author_sort | Shang, Guan-Sheng |
collection | PubMed |
description | The characteristics of cancer cells, such as invasiveness, are affected by the tumor microenvironment. Studies have shown that interleukin (IL)-6 and tumor necrosis factor (TNF)-α regulate the proliferation of lung cancer. However, few studies have focused on the effects of IL-6 and TNF-α on metastasis of lung cancer. The present study was designed to investigate whether IL-6 and TNF-α can promote metastasis of non-small cell lung cancer (NSCLC). Sixty-five tumor and matched adjacent tissue samples from patients with NSCLC and corresponding serum samples were collected. Thirty serum samples from healthy subjects were selected as controls. Real-time PCR and western blot analysis were used to measure IL-6, TNF-α, vimentin, E-cadherin, and N-cadherin expression in tissue samples; ELISA was used to measure IL-6 and TNF-α expression in serum samples. The correlation of serum levels of IL-6 and TNF-α with the clinical stage was analyzed; the correlation of IL-6 and TNF-α levels in serum with these tissues was analyzed; the correlation of serum levels of IL-6 and TNF-α with lymph node metastasis and distant metastasis was analyzed. Expression of IL-6 and TNF-α were significantly increased compared with controls in both serum and tissue; IL-6 and TNF-α levels were positively correlated with lymph node metastasis and distant metastasis; IL-6 and TNF-α levels were negatively correlated with E-cadherin level and were positively correlated with N-cadherin and vimentin levels. In conclusion, IL-6 and TNF-α can induce epithelial-mesenchymal transition, and subsequently promote metastasis of lung cancer. Anti-inflammation should be considered for the treatment of lung cancer. |
format | Online Article Text |
id | pubmed-5452994 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-54529942017-06-08 IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition Shang, Guan-Sheng Liu, Lunxu Qin, Yi-Wei Oncol Lett Articles The characteristics of cancer cells, such as invasiveness, are affected by the tumor microenvironment. Studies have shown that interleukin (IL)-6 and tumor necrosis factor (TNF)-α regulate the proliferation of lung cancer. However, few studies have focused on the effects of IL-6 and TNF-α on metastasis of lung cancer. The present study was designed to investigate whether IL-6 and TNF-α can promote metastasis of non-small cell lung cancer (NSCLC). Sixty-five tumor and matched adjacent tissue samples from patients with NSCLC and corresponding serum samples were collected. Thirty serum samples from healthy subjects were selected as controls. Real-time PCR and western blot analysis were used to measure IL-6, TNF-α, vimentin, E-cadherin, and N-cadherin expression in tissue samples; ELISA was used to measure IL-6 and TNF-α expression in serum samples. The correlation of serum levels of IL-6 and TNF-α with the clinical stage was analyzed; the correlation of IL-6 and TNF-α levels in serum with these tissues was analyzed; the correlation of serum levels of IL-6 and TNF-α with lymph node metastasis and distant metastasis was analyzed. Expression of IL-6 and TNF-α were significantly increased compared with controls in both serum and tissue; IL-6 and TNF-α levels were positively correlated with lymph node metastasis and distant metastasis; IL-6 and TNF-α levels were negatively correlated with E-cadherin level and were positively correlated with N-cadherin and vimentin levels. In conclusion, IL-6 and TNF-α can induce epithelial-mesenchymal transition, and subsequently promote metastasis of lung cancer. Anti-inflammation should be considered for the treatment of lung cancer. D.A. Spandidos 2017-06 2017-04-19 /pmc/articles/PMC5452994/ /pubmed/28599466 http://dx.doi.org/10.3892/ol.2017.6048 Text en Copyright: © Shang 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 Shang, Guan-Sheng Liu, Lunxu Qin, Yi-Wei IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition |
title | IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition |
title_full | IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition |
title_fullStr | IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition |
title_full_unstemmed | IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition |
title_short | IL-6 and TNF-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition |
title_sort | il-6 and tnf-α promote metastasis of lung cancer by inducing epithelial-mesenchymal transition |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452994/ https://www.ncbi.nlm.nih.gov/pubmed/28599466 http://dx.doi.org/10.3892/ol.2017.6048 |
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