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Fig. 1 | Infectious Agents and Cancer

Fig. 1

From: Hepatitis B virus X protein mediated suppression of miRNA-122 expression enhances hepatoblastoma cell proliferation through cyclin G1-p53 axis

Fig. 1

miR-122 expression is modulated by HBx in hepatoblastoma cells in vitro. a The relative expression of miR-122 in HepG2 cells transiently transfected with HBx expressing plasmid PCXN2-HBx or control vector. Cells are transfected with 1 μg and 2 μg of HBx plasmid respectively or pCXN2 as a control. b The relative expression of miR-122 in HepG2 cells transiently transfected with 1.3 fold full length HBV genome cloned into pUC19 plasmid or control vector. The cells are transfected with 1 μg pUC19-HBV or 1 μg pUC19. c The relative expression of miR-122 in constitutively HBV producing HepG2.2.15 cell line or control HepG2 cells. Cells were collected for analysis 48 h after each transfection. The miRNA expressions were measured by qRT-PCR. Plotted are the mean ± SD of three samples normalized to U6 expression (*P < 0.05, **P < 0.01, ***P < 0.001; Student’s t-test). d Real-time PCR analysis of miR-122 expression from patient serum samples. The miRNA levels in healthy controls were arbitrarily set as 1.0 and compared with advanced liver disease patients. e Comparison of miR-122 expression between healthy controls, LC and HCC patients. RNA was isolated from serum samples using miRVANA small RNA isolation assay and assayed using the TaqMan miRNA kit. The results were normalized to RNU6 endogenous control. Experiments were performed in triplicate. Error bars are means of ± standard deviation (SD). Mann–Whitney U test was performed to determine P-values (*P < 0.05, **P < 0.01, ***P < 0.001). LC = liver cirrhosis; HCC = Hepatocellular carcinoma

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