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. 2020 Mar 11;12(3):655. doi: 10.3390/cancers12030655

Figure 1.

Figure 1

HBV x protein (HBx) promoted the hepatocellular carcinoma (HCC) xenograft tumors growth via the upregulation of glycolytic metabolism in vivo. The HCC xenograft tumors with or without HBx-expressing were formed by Huh7-/MHCC-97H-pcDNA3.1-HA-HBx or Huh7-/MHCC-97H-pcDNA3.1-HA cells in BALB/c nude mice for 24 days. n = 6. (A) The growth curves of tumors were measured every two days. (B) Excised tumors were photographed after mice were sacrificed. (C) Tumor weights in the four groups. (D) The expression level of the cancer stemness related-proteins in the Huh7 xenograft tumors with or without HBx-expressing. The gray value of band was assessed by image-pro plus 6.0. The relative expression level was showed. (E) The mRNA levels of the cancer stemness-related genes in the Huh7 xenograft tumors with or without HBx-expressing. (F) Immunohistochemical staining of the cancer stemness-related proteins in the Huh7 xenograft tumors with or without HBx-expressing. Scale bar represents 50 μm. The levels of ATP content (G) and lactic acid (H) were detected in Huh7 and MHCC-97H xenograft tumors. (I) The mRNA levels of glycolysis-related genes in Huh7 xenograft tumors with or without HBx-expressing. The target gene transcription was normalized to ACTB. * P < 0.05 as compared with pc3.1-HA group. pc3.1-HA: pcDNA3.1-HA transfection without HBx-expressing. pc3.1-HA-HBx: pcDNA3.1-HA-HBx transfection with HBx-expressing.