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.
Highlights
Serum and glucocorticoid-inducible kinase (SGK)1is an AGC protein kinase of the SGK family, which can be triggered in response to a variety of physiological and pathological stimuli [1]
SGK1 transcription can be regulated by different signaling including cytosolic Ca2+, cyclic AMP, stress-activated protein kinase (SAPK2, p38 kinase), protein kinase C, and extracellular signalregulated kinase (ERK)1/2,and be activated by insulin, insulin-like growth factor (IGF)1, and hepatic growth factor (HGF) [8]
Sensitivity and specificity were better than for H. pylori infection and high-salt diet (HSD), which are well-known diagnostic indices of gastric cancer (GC) (H. pylori, area under the curve (AUC): 0.730, 95% confidence interval (CI):0.628–0.833; HSD, AUC: 0.640, 95% CI:0.529– 0.751) (Figure 5D). These results indicated that H. pylori infection and HSD induced SGK1 expression were ideal indicators in screening of GC
Summary
Serum and glucocorticoid-inducible kinase (SGK)1is an AGC protein kinase of the SGK family, which can be triggered in response to a variety of physiological and pathological stimuli [1]. SGK1 can be triggered by hyperosmotic cell shrinkage such as dehydration [2] and a modest increase of extracellular salt concentration [3]; and several hormones and mediators (cytokines), such as glucocorticoids [4], mineralocorticoids [5] transforming growth factor β [6] and interleukin (IL)-6 [7]. SGK1 can be enhanced in some pathological conditions, including diabetes, dialysis, glomerulonephritis, liver cirrhosis and malignancies [1]. SGK1 may support survival of tumor cells by counteracting apoptosis via phosphorylation, and inhibits glycogen synthase kinase 3, which downregulate oncogenic β-catenin [13, 14]
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