LAUSR

In the present study, we proposed to investigate the role of miR-122 in hepatocarcinoma progression and to explore the mechanism. In hepatocarcinoma tissues and cells, we used qRT-PCR to validate the miR-122 expression level. Next, we used colony formation by crystal violet staining assay to compare cell proliferation ability, and we used scratch test or transwell assay to compare cell migration or invasion ability. And then we conducted bioinformatics or luciferase reporter gene assay to prove the regulation effect of miR-122 on lamin B2 (LMNB2), and the biological function of LMNB2 was analyzed. At last we used nude mouse tumorigenicity assay to test the inhibition effect of miR-122 ASO therapy against hepatocarcinoma. MiR-122 was reduced in hepatocarcinoma tissues compared to the para-carcinoma tissues, which was relatively low or high in hepatocarcinoma cell line SMMC7721 or Hep3B, and over-expressed miR-122 inhibited proliferation, migration or invasion in hepatocarcinoma cells. Additionally, some reports showed that LMNB2 was regulated by miR-122, which inhibited the expression of LMNB2. Moreover, LMNB2 was functioning to promote cell proliferation, migration and invasion. At last we could achieve the inhibition of hepatocarcinoma by using miR-122 therapy through decreasing LMNB2 expression in vivo. Our data indicated that miR-122 could inhibit hepatocellular carcinoma cell progression by targeting LMNB2 and as a therapeutic target for hepatocarcinoma treatment.