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. 2021 Sep 10;6(1):209–222. doi: 10.1002/hep4.1724

FIG. 6.

FIG. 6

SLC45A2‐AMACR induced spontaneous liver cancer. (A) Schematic diagram of the hydrodynamic injection of pT3‐SLC45A2‐AMACR‐FLAG/pSB to induce liver cancer in C57Blloxp‐Pten‐Loxp mice treated with AAV8‐cre. (B) Representative picture of mouse liver treated with pT3/pSB or pT3‐SLC45A2‐AMACR‐FLAG/pSB (0.5 images). Liver cancer nodules are indicated by green arrows. (C) Hematoxylin and eosin staining of liver samples from pT3‐SLC45A2‐AMACR‐FLAG/pSB‐treated (9 weeks) mice (top, 4x images) or pT3/pSB‐treated (9 weeks) mice (bottom, 20x images). Liver cancer is indicated by green arrows. Middle panels represent the high magnification (20x) images of the indicated areas of the top panel. (D) SLC45A2‐AMACR increased the liver to body ratio. Data show mean ± SD.(E) SLC45A2‐AMACR‐FLAG increased Ki67‐positive cells in liver cancer (20x images). (F) SLC45A2‐AMACR‐FLAG enhanced the activation of ERK kinase and its signaling molecules MEK and mTOR kinases. Abbreviations: AAV8, adeno‐associated virus 8; HPF, high‐power field.