Fig. 8.

Adeno-associated virus based on serotype 8 (AAV8)-medicated Aldoa deficiency decreased the susceptibility of mice to diethylnitrosamine (DEN)-induced hepatocellular carcinoma (HCC). (A) Schematic treatment of DEN challenge (intraperitoneally) and AAV8 intervention (intravenously) on male C57BL/6 mice. (B) Representative images of livers at 8 months after DEN treatment. (C) Quantification of the liver-to-body weight ratios (n = 8). (D) The number of macroscopic tumors (≥0.1 cm) identified in animals at the time of sacrifice (n = 8). (E) The mean max tumor volumes in three groups (n = 8). (F) Representative images of hematoxylin and eosin (H&E) staining in tumor foci and adjacent normal liver. Some tumors in the livers are shown by dotted circles. (G) Representative images of Ki67 immunohistochemistry staining and quantification in tumor foci and adjacent normal liver (n = 12). (H–J) The levels of glucose (H), lactate (I), and glycosylated serum protein (GSP) (J) in the serum of DEN-induced mice (n = 6). (K) The protein levels of aldolase A (ALDOA), phosphorylated c-Jun (p-c-Jun) Thr93, c-Jun, and P21-activated kinase 2 (PAK2) in the livers of DEN-treated mice (n = 4). (L) The messenger RNA (mRNA) levels of Cxcl1, Dusp1, Fgb, and Ppp1r15a in the livers of DEN-treated mice (n = 6). N.S.: no significant difference, ^∗P < 0.05, ^∗∗P < 0.01, ^∗∗∗P < 0.001. WT: wild-type, AAV8-shAldoa: AAV8 liver-specific Aldoa knockdown; AAV8-GFP: AAV8 liver-specific GFP control; IOD: integrated optical density.