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

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Abstract

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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Yin, Y., Si, X., Gao, Y., Gao, L., & Wang, J. (2013). The nuclear factor-?B correlates with increased expression of interleukin-6 and promotes progression of gastric carcinoma. Oncology Reports, 29(1), 34–38. https://doi.org/10.3892/or.2012.2089

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