Lnc-SGK1 induced by Helicobacter pylori infection and highsalt diet promote Th2 and Th17 differentiation in human gastric cancer by SGK1/Jun B signaling

// Yongliang Yao 1 , Qingbo Jiang 2 , Lixing Jiang 3 , Jianhong Wu 1 , Qinghui Zhang 1 , Jianjun Wang 1 , Huang Feng 1 , Panpan Zang 1 1 Department of Clinical Laboratory, The First People’s Hospital of Kunshan, Affiliated to Jiangsu University, Kunshan, Jiangsu, China 2 Department of Clinical Laboratory, The Third Affiliated Hospital of Suzhou University, Changzhou, Jiangsu, China 3 Department of Clinical Laboratory, Wujin Hospital Affiliated to Jiangsu University, Changzhou, Jiangsu, China Correspondence to: Yongliang Yao, e-mail: Yaoyl313@163.com 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 ABSTRACT 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.