1 After binding to target mRNAs, miRNAs form a complex with them and reduce their protein levels, either by degrading the mRNA or by suppressing the translation of the target gene.2 It has been reported that miRNAs can posttranscriptionally regulate ≈30% of human genes, suggesting that miRNAs may have pivotal roles in physiological and find more pathological processes,

including human carcinogenesis.3 Over the past 5 years, emerging evidence has demonstrated that miRNAs are crucial for the initiation, promotion, and progression of human cancers. For example, miR-15a and miR-16-1 were first investigated in tumorigenesis and found to be frequently translocated or deleted in chronic lymphocytic leukemia.4 It has been reported that AAV-mediated miR-26a had therapeutic effects Compound Library order in vivo in a

murine liver cancer model.5 Recently, Trang et al.6 found that loss of tumor suppressor let-7 could facilitate the progression of lung tumors in mice, and exogenous delivery of let-7 into established lung tumors in mice remarkably inhibited tumor growth. These findings suggest that tumor-suppressive miRNAs can be delivered in vivo to suppress tumor growth, thus providing a new strategy for cancer therapy. Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide and is the third most common cause of cancer-related death.7 China alone accounts for more than 50% of HCC incidence in the world.8 The molecular pathogenesis of HCC is complicated and poorly understood. Although previous studies have suggested that many protein-coding genes are

involved in the development and progression of HCC,9 the roles and potential mechanisms of miRNAs in HCC are largely unexplored. In a previous report, our miRNA profiling result showed that 84 miRNAs were differentially expressed in HCC versus nontumorous liver tissues, and only miR-125b expression was associated with patients’ survival.10 Recent studies have demonstrated that miR-125b is dysregulated in multiple types of cancer, including breast,11 oral,12 bladder,13 and anaplastic see more thyroid carcinomas.14 These findings indicate that miR-125b may function importantly in human carcinogenesis. However, the possible roles and mechanisms of miR-125b in human HCC are still not well established. In this study, we found that expression of miR-125b was suppressed in about 70% of primary HCCs and was highly associated with Ki-67 expression. miR-125b could inhibit cell proliferation, cell cycle progression and metastasis of HCC cells. Moreover, the oncogene LIN28B was identified as a direct and functional target for miR-125b in hepatic carcinogenesis. 3′-UTR, 3′ untranslated region; HCC, hepatocellular carcinoma; miRNA, microRNA; mRNA, messenger RNA; PCR, polymerase chain reaction; qRT-PCR, quantitative reverse-transcription polymerase chain reaction; siRNA, small interfering RNA. Total RNA was extracted with TRIzol reagent (Invitrogen, CA).