Fig.4.
HK2-stimulated glycolysis mediates the UBR7 deficiency-induced metastatic and invasive phenotype. A Western blot detected Huh-7 cells stably overexpress UBR7 and HK2. B-D Glycolysis rate, ATP level, cell migration and clone formation ability were detected in Huh-7 cells overexpressing UBR7 or/and HK2. (E) Left: Xenograft tumour and tumour weight were constructed by the subcutaneous injection of Huh-7 cells overexpressing UBR7 and HK2 alone or together. Right: incidence of LN metastasis and Lymph node size level after Huh-7 cell tail vein injection. (F)Western blot detected HepG2 cells knockout UBR7 or/and HK2. G-I Glycolysis rate, ATP level, cell migration and clone formation ability were detected in HepG2 cells with the knockout of UBR7 or/and HK2. J Left: Xenograft tumour and tumour weight were constructed by subcutaneous injection of HepG2 cells knocking-out UBR7 and HK2 alone or together. Right: incidence of LN metastasis and Lymph node size level after HepG2 cells knocking-out UBR7 and HK2 alone or together in the tail vein injection. Data are shown as mean ± SD of three independent experiments. *p < 0.05, **p < 0.01. The scale bar in (D) and (I) was 100 μm