Since previous studies have shown that the expression of miR-454 was significantly up-regulated in colon cancer and in HCT116 cells, and miR-454 contributed to colon tumorigenesis by directly repressing the expression of Smad4 [13], we further investigated whether Smad4 was also a direct target of miR-454 to regulate the expression of α-SMA in TGF-β1-treated LX-2 cells. This evidence concerns the gene ACTA1 and colonic neoplasm.