Fig. 8: ACLY K468-Ac confers HCC cells and mouse xenografts chemoresistance. | Cell Death & Disease

Fig. 8: ACLY K468-Ac confers HCC cells and mouse xenografts chemoresistance.

From: Chemotherapy-induced acetylation of ACLY by NAT10 promotes its nuclear accumulation and acetyl-CoA production to drive chemoresistance in hepatocellular carcinoma

Fig. 8

A WB was performed on the cell lysates to evaluate GFP-ACLY levels in GFP, GFP-ACLY, and GFP-ACLY K468R stable expression Huh7 cells. B The IC50 of doxorubicin and oxaliplatin in the GFP, GFP-ACLY, and GFP-ACLY K468R stable expression Huh7 cells. Data were analyzed by one-way ANOVA and presented as mean ± SD (n = 3). C GFP, GFP-ACLY, and GFP-ACLY K468R stable expression Huh7 cells were subcutaneously implanted into nude mice (n = 6). Oxaliplatin (5 mg/kg) was intraperitoneally injected twice a week after Huh7 cells injection. D The volumes of the tumor xenografts were shown, respectively. Data were analyzed by one-way ANOVA and presented as mean ± SD, ***P < 0.001. E Tumors were dissected at the end of the experiment. F HE staining was performed with these tumor tissues. Scale bar, 50 μm. G The weights of the tumor xenografts were shown, respectively. Data were analyzed by one-way ANOVA and presented as mean ± SD, ns denotes no significance, ***P < 0.001. H Proteins extracted from the xenografts were subjected to Western blot probed with anti-GFP-ACLY, anti-PIK3R1, and anti-CYP2C9 antibodies. Beta-actin was used as a loading control. I WB analysis of ACLY K468-Ac expression in 6 individual paired HCC tissues. J A working model explaining the mechanism by which NAT10 leads to chemoresistance.

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