Lnc-SGK1 induced by Helicobacter pylori infection and highsalt diet promote Th2 and Th17 differentiation in human gastric cancer by SGK1/Jun B signaling
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Yongliang Yao1, Qingbo Jiang2, Lixing Jiang3, Jianhong Wu1, Qinghui Zhang1, Jianjun Wang1, Huang Feng1, Panpan Zang1
1Department of Clinical Laboratory, The First People’s Hospital of Kunshan, Affiliated to Jiangsu University, Kunshan, Jiangsu, China
2Department of Clinical Laboratory, The Third Affiliated Hospital of Suzhou University, Changzhou, Jiangsu, China
3Department of Clinical Laboratory, Wujin Hospital Affiliated to Jiangsu University, Changzhou, Jiangsu, China
Yongliang Yao, e-mail: [email protected]
Keywords: gastric cancer, high-salt diet, Helicobacter pylori infection, serum and glucocorticoid-inducible kinase, LncRNA
Received: December 07, 2015 Accepted: February 14, 2016 Published: March 01, 2016
Serum and glucocorticoid-inducible kinase (SGK) 1can be triggered in several malignancies. Most research on SGK1has focused on its role in cancer cells, and we sought to investigate its potential upstream non-coding RNA nominated as Lnc-SGK1, and their expression and diagnostic value in T cells in human gastric cancer (GC). Excessive expression of Lnc-SGK1 and SGK1 were observed in T cell either within the tumor or peripheral T cells, and furthermore associated with Helicobacter pylori infection and high-salt diet (HSD). Within T cells, Helicobacter pylori (Hp) infection and high-salt dietcan up-regulated SGK1 expression and in turn enhance expression of Lnc-SGK1 through JunB activation. And expression of Lnc-SGK1 can further enhance transcription of SGK1 through cis regulatory mode. Lnc-SGK1 can induce Th2 and Th17 and reduce Th1 differentiation via SGK1/JunB signaling. Serum Lnc-SGK1 expression in combination with H. pylori infection and/or HSD in T cells was associated with poor prognosis of GC patients, and could be an ideal diagnostic index in human GC.
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