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The nuclear factor-κB correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma

The interleukin-6 (IL-6) pathway is one of the mechanisms that link inflammation and angiogenesis with malignancy. Since nuclear factor-κB (NF-κB) is a potential sign for inflammation, NF-κB has been associated with the progression of disease in various types of cancer. In the present study, we inve...

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Autores principales: YIN, YEFENG, SI, XIULIAN, GAO, YAN, GAO, LEI, WANG, JIANGNING
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3583490/
https://www.ncbi.nlm.nih.gov/pubmed/23117246
http://dx.doi.org/10.3892/or.2012.2089
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author YIN, YEFENG
SI, XIULIAN
GAO, YAN
GAO, LEI
WANG, JIANGNING
author_facet YIN, YEFENG
SI, XIULIAN
GAO, YAN
GAO, LEI
WANG, JIANGNING
author_sort YIN, YEFENG
collection PubMed
description The interleukin-6 (IL-6) pathway is one of the mechanisms that link inflammation and angiogenesis with malignancy. Since nuclear factor-κB (NF-κB) is a potential sign for inflammation, NF-κB has been associated with the progression of disease in various types of cancer. In the present study, we investigated the effect of NF-κB on the IL-6 pathway in gastric carcinoma and their correlation with disease status and prognosis. The mRNA and protein levels of NF-κB, IL-6 and vascular endothelial growth factor (VEGF) were detected by western blotting and reverse transcription (RT) quantitative PCR (RT-qPCR). Using immunohistochemistry, we examined the expression of these proteins in normal and human gastric cancer tissue samples. The concentrations of IL-6 and TNF-α in collected blood samples were measured according to the enzyme-linked immunosorbent assay (ELISA). IL-6 and TNF-α were found to be expressed at high levels in human gastric cancer samples. A positive correlation was found between the expression of IL-6 and NF-κB by immunohistochemical and further correlation analysis. IL-6, NF-κB and VEGF protein and mRNA levels increased significantly in gastric cancer tissue compared with those in adjacent normal mucosa tissue samples. In conclusion, our findings demonstrate that NF-κB, IL-6 and VEGF mRNA and protein levels increase significantly in gastric cancer tissues. In addition, the expression of NF-κB was positively correlated with the expression of IL-6 according to immunohistochemical and further correlation analysis, which suggests that the suppression of NF-κB or IL-6 may be a potential target for clinical therapy of gastric cancer in the future.
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spelling pubmed-35834902013-02-28 The nuclear factor-κB correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma YIN, YEFENG SI, XIULIAN GAO, YAN GAO, LEI WANG, JIANGNING Oncol Rep Articles The interleukin-6 (IL-6) pathway is one of the mechanisms that link inflammation and angiogenesis with malignancy. Since nuclear factor-κB (NF-κB) is a potential sign for inflammation, NF-κB has been associated with the progression of disease in various types of cancer. In the present study, we investigated the effect of NF-κB on the IL-6 pathway in gastric carcinoma and their correlation with disease status and prognosis. The mRNA and protein levels of NF-κB, IL-6 and vascular endothelial growth factor (VEGF) were detected by western blotting and reverse transcription (RT) quantitative PCR (RT-qPCR). Using immunohistochemistry, we examined the expression of these proteins in normal and human gastric cancer tissue samples. The concentrations of IL-6 and TNF-α in collected blood samples were measured according to the enzyme-linked immunosorbent assay (ELISA). IL-6 and TNF-α were found to be expressed at high levels in human gastric cancer samples. A positive correlation was found between the expression of IL-6 and NF-κB by immunohistochemical and further correlation analysis. IL-6, NF-κB and VEGF protein and mRNA levels increased significantly in gastric cancer tissue compared with those in adjacent normal mucosa tissue samples. In conclusion, our findings demonstrate that NF-κB, IL-6 and VEGF mRNA and protein levels increase significantly in gastric cancer tissues. In addition, the expression of NF-κB was positively correlated with the expression of IL-6 according to immunohistochemical and further correlation analysis, which suggests that the suppression of NF-κB or IL-6 may be a potential target for clinical therapy of gastric cancer in the future. D.A. Spandidos 2012-10-19 2013-01 /pmc/articles/PMC3583490/ /pubmed/23117246 http://dx.doi.org/10.3892/or.2012.2089 Text en Copyright © 2013, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Articles
YIN, YEFENG
SI, XIULIAN
GAO, YAN
GAO, LEI
WANG, JIANGNING
The nuclear factor-κB correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma
title The nuclear factor-κB correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma
title_full The nuclear factor-κB correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma
title_fullStr The nuclear factor-κB correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma
title_full_unstemmed The nuclear factor-κB correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma
title_short The nuclear factor-κB correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma
title_sort nuclear factor-κb correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3583490/
https://www.ncbi.nlm.nih.gov/pubmed/23117246
http://dx.doi.org/10.3892/or.2012.2089
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