Resistin-Like Molecule-β Promotes Invasion and Migration of Gastric Carcinoma Cells

BACKGROUND: Resistin-like molecule-β (RELMβ) is a novel secretory protein from intestinal goblet cells and participates in epithelial differentiation, tumor occurrence, and immune response. RELMβ is absent in normal gastric mucosa but is abundantly expressed in gastric carcinoma tissues, and is correlated with tumor invasion and metastasis. Epithelial-mesenchymal transition (EMT) is an important mechanism governing tumor cell invasion. This study thus investigated the modulation of RELMβ in gastric cancer metastasis and its correlation with EMT. MATERIAL/METHODS: We used RELMβ-low expression AGS cell line of gastric cancer and normal mucosa cell line GES1 as in vitro models, on which RELMβ0-expressing vector was transfected. The invasion and migration of cells were quantified by Transwell assay. EMT-related protein including E-cadherin, N-cadherin, Snail, and Vimentin were detected by Western blotting in transfected AGS cells. RESULTS: RELMβ transfection significantly potentiated invasion and migration abilities of AGS cells, whose RELMβ protein level was significantly elevated compared to those in untransfected AGS or GES1 cells. After RELMβ transfection, EMT-related proteins, including N-cadherin, Snail, and Vimentin levels, were elevated, but E-cadherin expression was depressed. CONCLUSIONS: RELMβ-overexpression can facilitate invasion and migration of gastric carcinoma cells and it increases the expression of EMT-related proteins, such as N-cadherin, Snail, Vimentin, but decreases E-cadherin level, thus promoting the progression of EMT.