epstein-barr virus-induced gene 3 (ebi3) blocking leads to induce antitumor cytotoxic t lymphocyte response and suppress tumor growth in colorectal cancer by bidirectional reciprocal-regulation stat3 signaling pathway

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ID: 161701
2016
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Abstract
Epstein-Barr virus-induced gene 3 (EBI3) is a member of the interleukin-12 (IL-12) family structural subunit and can form a heterodimer with IL-27p28 and IL-12p35 subunit to build IL-27 and IL-35, respectively. However, IL-27 stimulates whereas IL-35 inhibits antitumor T cell responses. To date, little is known about the role of EBI3 in tumor microenvironment. In this study, firstly we assessed EBI3, IL-27p28, IL-12p35, gp130, and p-STAT3 expression with clinicopathological parameters of colorectal cancer (CRC) tissues; then we evaluated the antitumor T cell responses and tumor growth with a EBI3 blocking peptide. We found that elevated EBI3 may be associated with IL-12p35, gp130, and p-STAT3 to promote CRC progression. EBI3 blocking peptide promoted antitumor cytotoxic T lymphocyte (CTL) response by inducing Granzyme B, IFN-γ production, and p-STAT3 expression and inhibited CRC cell proliferation and tumor growth to associate with suppressing gp130 and p-STAT3 expression. Taken together, these results suggest that EBI3 may mediate a bidirectional reciprocal-regulation STAT3 signaling pathway to assist the tumor escape immune surveillance in CRC.
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liang2016mediatorsepstein-barr Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Yanfang Liang;Qianqian Chen;Wenjing Du;Can Chen;Feifei Li;Jingying Yang;Jianyu Peng;Dongping Kang;Bihua Lin;Xingxing Chai;Keyuan Zhou;Jincheng Zeng
Journal polyhedron
Year 2016
DOI
10.1155/2016/3214105
URL
http://dx.doi.org/10.1155/2016/3214105
Keywords
pathology

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