| Increased expression of Gal-1in CAFs cells had been reported to correlate with the progression and prognosis in many cancers. However, rare reports have sought to determine whether high Gal-1expression in CAFs 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 primary cultured the gastric cancer CAFs, which shows strong expression of Gal-1, and established a co-culture system of CAFs with gastric cancer cell. The specific siRNA and in vitro migration and invasion assay were used to explore the effects of the interaction between Gal-1expression of CAFs and gastric cancer cells on cell migration and invasion. We found that the over-expression of Gal-1in CAFs enhanced gastric cancer cell migration and invasion, and these stimulatory effects could be blocked by specific siRNA which reduced the Gal-1expression level.Then, a set of cancer invasion-associated genes were chosen to identify the possible mechanism of Gal-1-induced cell invasion. Among these genes, integrin β1expression in cancer cells was considered to be associated with Gal-1expression. Pre-blocking of the integrin β1expression in gastric cancer cells with siRNA could interrupt the invasion-promoting effect of CAFs with high Gal-1expression. Furthermore, IHC assay confirmed a positive correlation between Gal-1and integrin β1expression.In conclusion, our results showed that high expression of Gal-1in CAFs might facilitate gastric cancer cell migration and invasion by up-regulating the integrin β1expression in gastric cancer. |
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