Aberrant activation of the Wnt/β-catenin signal pathway is frequently observed 
in hepatocellular carcinoma (HCC). β-Catenin is the major cellular effector of 
Wnt signaling and inactivation of adenomatous polyposis coli (APC) results in 
nuclear accumulation of β-catenin. Therefore, it was speculated that APC 
inhibition could play important roles in activating the Wnt/β-catenin pathway 
and in HCC progression. In this study, we report that miR-106b expression is 
markedly upregulated in hepatoma cells and hepatoma tissues compared with 
immortalized normal liver epithelial cells and normal hepatic tissues. Ectopic 
expression of miR-106b induces the proliferation and anchorage-independent 
growth of hepatoma cells, whereas inhibition of miR-106b reduced this effect. 
Furthermore, miR-106b upregulation in hepatoma cells modulated entry into the 
G(1)/S transitional phase by upregulating cyclin D1 and downregulating APC. 
Moreover, we demonstrated that miR-106b downregulates APC expression by directly 
targeting the 3'-untranslated region of APC messenger RNA. Taken together, our 
results suggest that miR-106b plays an important role in promoting the 
proliferation of human hepatoma cells and presents a novel mechanism of micro 
RNA-mediated direct suppression of APC expression in cancer cells.