Hepatocellular carcinoma (HCC) is one of the most common malignancies and 
exhibits heterogeneity in terms of clinical outcomes and biological activities. 
Emerging evidence has demonstrated that cancer stem cells (CSCs) play important 
roles in the tumorigenesis and progression of HCC. However, the molecular 
mechanisms underlying the stemness maintenance of CSCs remain largely unknown. 
In the present study, through real-time PCR, western blotting, luciferase 
assays, RNA immunoprecipitation, and in vitro and in vivo assays, we 
demonstrated that miR-217 expression was markedly increased in HCC tissues and 
cells. Overexpression of miR-217 promoted, while silencing miR-217 suppressed, 
the fraction of the side population and the expression of cancer stem cell 
factors in vitro and tumorigenicity in vivo in HCC cells. Our findings further 
demonstrated that miR-217 promoted the CSC-like phenotype via dickkopf-1 (DKK1) 
targeting, resulting in constitutive activation of Wnt signaling. Moreover, the 
stimulatory effects of miR-217 on stem cell properties and Wnt signaling were 
antagonized by the upregulation of DKK1 in miR-217-overexpressing cells. 
Conversely, the inhibitory effects of silencing miR-217 on stem cell properties 
and Wnt signaling were reversed by the downregulation of DKK1 in 
miR-217-downregulated cells. Therefore, our results indicate that miR-217 plays 
a vital role in the CSC-like phenotypes of HCC cells and may be used as a 
potential therapeutic target against HCC.