Hepatocellular carcinoma (HCC), one of the most common cancers worldwide, represents the third cause of cancer-related death1. Curative options for HCC are limited and exclusively available for patients carrying an early stage HCC. In advanced stages, traditional chemotherapy proved to be only marginally effective or even toxic. Thus, the identification of new treatment options is needed. New targets for non-conventional treatment will necessarily take advantage of progresses on the molecular pathogenesis of HCC2.

MicroRNAs (miRNAs) are short non-coding RNAs 19–25 nucleotides in length, which negatively regulate gene expression by pairing with complementary sequences within the 3′-untranslated regions (UTRs) of targeted transcripts at the post-transcriptional and/or translational level3, 4. miRNAs expression is frequently deregulated in many types of human cancers, and plays critical roles in tumorigenesis, which functions either as tumor suppressors or as oncogenes. In the recent years, several studies have revealed that the expression of miRNAs is deregulated in human HCC in comparison with matched non-neoplastic tissue5. More and more miRNAs involved in hepatocarcinogenesis were identified in HCC tissues. Xu et al indicated that miR-195 may suppress tumorigenicity and regulate G1/S transition of HCC cells by repressing Rb-E2F signaling involving targeting multiple molecules, such as cyclin D1, CDK6, and E2F36. Liang et al reported that miR-125b was able to suppress tumor growth in hepatic carcinogenesis through the suppression of oncogene LIN28B expression7. miR-637 acts as a tumor suppressor, through the suppressive effect on HCC mediated by disruption of Stat3 activation8. miR-99a acts as a prospective prognosis predictor of HCC and potential tumor suppressor for HCC therapeutics, which induces cell cycle arrest by directly targeting IGF-1R and mTOR9. Thus, those miRNAs may function in a network in hepatocarcinogenesis.

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