This finding was further supported by the finding that the over-expression of miR-199a repressed tumor formation and growth in nude mice. In fact, a miRNA is usually down-regulated in a particular human cancer and can have tumor-suppressor-like effects if the main targets for that specific cell type are oncogenes. It is generally accepted that miRNAs exert their function through regulating the expression of their downstream BMN673 target genes. We integrated bioinformatic algorithms, including miRanda, PicTar and TargetScan, to identify the potential target genes of miR-199a. Among the potential mRNAs targeted by miR-199a, FZD7 was particularly interesting. Previous studies indicated that a functional interaction between FZD7 and Wnt3 leads to activation of the Wnt/b-catenin signaling pathway in HCC cells and may play an important role in hepatocarcinogenesis. Among the FZD family, FZD7 appears to be the most important Wnt receptor involved in cancer development and progression, and FZD7 is most commonly up-regulated in a variety of cancers, including colorectal cancer, HCC, esophageal cancer, breast cancer, lung cancer, Wilm’s tumor, gastric cancer and melanoma. The over-activation of Wnt signaling with the up-regulated expression of FZD7 in various types of cancer and the roles of FZD7 in cancer stem cell biology suggest that FZD7 might serve as a therapeutic target for certain cancers. Several research groups have attenuated the action of over-expressed Fzd7 in cancer cells using different methods such as an anti-FZD7 antibody, an extracellular peptide of FZD7, small interfering peptides or a small molecule inhibitor. Therefore, targeted inhibition of FZD7 represents a rational and promising new approach for cancer therapy. To experimentally validate this computer prediction, luciferase reporter assays confirmed that FZD7 was a target gene of miR-199a. These data were further strengthened by results from exploring the protein levels of FZD7 in HepG2 cells by western blotting, which showed that the over-expression of miR-199a markedly decreased FZD7 protein expression. Then, the downstream genes of FZD7, including b-catenin, Jun, Cyclin D1 and Myc were investigated using western blot analysis, and the results demonstrated that over-expression of miR-199a could significantly down-regulate the expression of the downstream genes of FZD7. Moreover, the co-expression of miR-199a and its target gene FZD7 were detected in HCC tissues. The results showed that miR-199a was inversely correlated with FZD7 expression in HCC tissues. Taken together, these results strongly suggested that miR-199a might function as a tumor suppressor partly by mediating the repression of FZD7 expression in HCC development. In conclusion, the data presented here strongly indicate that miR-199a acts as a tumor suppressor in HCC. Our present study showed that miR-199a is frequently down-regulated and inversely correlated with poor prognosis in HCC patients. In addition, restoration of miR-199a expression in HCC cells leads to inhibition of the cell proliferation and of the cell cycle partly through down-regulating FZD7 in vitro and in vivo. These findings not only help us to better elucidate the molecular mechanisms of hepatocarcinogenesis from a fresh perspective but also provide a new theoretical basis to further investigate miR199a as a potential biomarker and a promising approach for HCC treatment. Currently, surgical resection is still the main method to prolong the survival time of lung cancer, but the invasion and metastasis of lung cancer is the biggest obstacle to improve the efficacy of the prognosis of lung cancer.