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In addition, CCAT1-shRNA significantly reduced vascular endothelial growth factor (VEGF) expression in SW480 cells; however, these effects were partially rescued by an miR-218 inhibitor. Furthermore, it was revealed that the CCAT1-plasmid significantly promoted the viability of SW480 cells, increased cell migration and invasiveness, and significantly increased VEGF expression. However, these effects were also partially rescued by with a miR-218 mimic. Taken together, the present results identified that the CCAT1/miR-218 axis serves a key r
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