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Increased expression of galectin‐1 ( G al‐1) in carcinoma‐associated fibroblasts ( CAF s) has been reported to correlate with progression and prognosis in many cancers. However, rarely have reports sought to determine whether high  G al‐1 expression in  CAF s in gastric cancer is involved in the tumor process, and the specific mechanism by which it promotes the evolution of gastric cancer is still unknown. In this study, we cultured gastric cancer  CAF s, which showed strong expression of  G al‐1, and established a co‐culture system of  CAF s with gastric cancer cells. Specific si RNA  and  in vitro  migration and invasion assays were used to explore the effects of the interaction between  G al‐1 expression of  CAF s and gastric cancer cells on cell migration and invasion. We found that the overexpression of  G al‐1 in  CAF s enhanced gastric cancer cell migration and invasion, and these stimulatory effects could be blocked by specific si RNA  which reduced the  G al‐1 expression level. A set of cancer invasion‐associated genes were then chosen to identify the possible mechanism of  G al‐1‐induced cell invasion. Among these genes,  integrin  β 1  expression in cancer cells was considered to be associated with  G al‐1 expression. Pre‐blocking of the integrin β1 expression in gastric cancer cells with si RNA  could interrupt the invasion‐promoting effect of  CAF s with high  G al‐1 expression. Furthermore, immunohistochemical assay confirmed a positive correlation between  G al‐1 and integrin β1 expression. Our results showed that high expression of  G al‐1 in  CAF s might facilitate gastric cancer cell migration and invasion by upregulating integrin β1 expression in gastric cancer.

Expression of galectin‐1 in carcinoma‐associated fibroblasts promotes gastric cancer cell invasion through upregulation of integrin β1