High MIG-6 expression promotes tumor proliferation and metastasis of gastric cancer

<b>Background:</b> Mitogen-inducible gene-6 (<i>MIG-6</i>) is a feedback inhibitor that targets activated epidermal growth factor receptor (EGFR) and suppresses tumor growth fueled by constitutively activated EGFR. Nevertheless, the action mechanism of <i>MIG-6</i> in gastric cancer (GC) remains to be elucidated. <b>Methods:</b> Western blotting, fluorescence quantitative PCR, and immunohistochemistry were performed to detect the expression of <i>MIG-6</i> in GC cell lines and tissues. Public databases were used to analyze <i>MIG-6</i> in patients with GC. Furthermore, the GC cell lines were selected for the knockdown and overexpression of <i>MIG-6</i>. <b>Results:</b> Bioinformatics and histological analyses showed that <i>MIG-6</i> was elevated in human GC tissues and cells. The Kaplan-Meier plotter showed that patients with elevated MIG-6 expression had significantly shorter survival. Furthermore, small interference RNA-mediated reduction of <i>MIG-6</i> expression decreased EGFR/AKT signaling, as well as the proliferation and metastasis of human GC cells <i>in vitro</i>, whereas its overexpression increased these actions. Also, <i>MIG-6</i> overexpression promoted the epithelial-mesenchymal transition of GC cells as well as the expression of the migration-associated protein matrix metalloproteinase-9 <i>in vitro</i>. <b>Conclusion:</b> These results suggest that <i>MIG-6</i> can serve as a new prognostic biomarker or potential therapeutic target for the identification of patients with poor survival.