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Fig. 2 | Infectious Agents and Cancer

Fig. 2

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

Fig. 2

HBx modulated expression of target mRNA and protein CCNG1 (cyclin G1) in hepatoblastoma cells. a Relative expression of CCNG1 mRNA– target of miR-122 in HBx transfected HepG2 cells. Cells are transfected with 1 μg and 2 μg of pCXN2-HBx respectively or pCXN2 as a control. b Relative expression of CCNG1 mRNA in 1.3 fold full length HBV genome transfected HepG2 cells. Cells are transfected with 1 μg pUC19-HBV or 1 μg pUC19 control vector. c Relative expression of CCNG1 mRNA in HepG2.2.15 cell line and in control HepG2 cells. RNA were extracted 48 h post transfection. The mRNA expressions were measured by qRT-PCR and the expressions were normalized to GAPDH. Data are expressed as the mean ± SD from three independent experiments (*P < 0.05, **P < 0.01, ***P < 0.001; Student’s t-test). d Western blot confirmed protein cyclin G1 was increased accordingly in HBx transfected HepG2 cells. HepG2 cells are transfected with 1 μg and 2 μg of pCXN2-HBx respectively or empty pCXN2 as a control. e Expression of cyclin G1 protein in 1.3 fold HBV transfected HepG2 cells. HepG2 cells are transfected with 1 μg pUC19-HBV or 1 μg pUC19 vector as a control. f Expression of cyclin G1 in constitutively HBV producing HepG2.2.15 and control HepG2 cell line. Cells were collected for protein analysis 48 h after each transfection. β actin was taken as endogenous control. Protein bands were quantified using Densitometric scanner (Bio-Rad). Below are the graphical representations of intensity ratio between target protein cyclin G1 and β actin in each lane

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