Figure 8.

miR-520c-3p antagomir inhibition of HBX-induced tumor progression in vivo

(A) qPCR and western blot assays showed a significantly higher expression of HBx in a stable HBx-overexpression HepG2 cell line. (B) Mice were imaged with live image equipment. The relative fluorescence intensity of the mice was calculated by using ImageJ, and the scatter diagram was drawn by using GraphPad Prism software. (C) Expression of PTEN and miR-520c-3p in tumors with NC/miR-520c-3p-antagomir-treatment were analyzed by qPCR. (D) Proteins in the AKT/NF-κB pathway were analyzed in tumor tissues by western blot. (E) Representative live images of mouse livers and lungs. (F) A model for HBV-induced cell migration and invasion. HBV, via HBx binding to CREB1, upregulates miR-520c-3p, which in turn downregulates PTEN, thereby leading to the activation of AKT/NF-κB pathway to enhance HCC EMT and thus cell migration and invasion. This study reveals that miR-520c-3p, upregulated by HBx of HBV, targets PTEN, an anti-oncogene, to promote hepatoma cell migration and metastasis through the activation of AKT/NF-κB pathway. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.