Fig. 6: Slc13a3 deficiency inhibits the growth of β-catenin-activated HCCs.

a Cell viability of HepG2 and SNU398 cells. Stably control (sgControl, gray curve) and SLC13A3-deficient (sgSLC13A3, blue curve) cells were established by infection with CRISPR/Cas9 sgControl or sgSLC13A3 lentivirus, respectively. For re-expression study, sgControl and sgSLC13A3 cells were transfected with empty vector (EV, red)- or SLC13A3-overexpressing (purple) plasmids for 24 h. Cell viability was determined at the indicated time points. Data are presented as the mean ± SEM (n = 3 independent experiments). Statistical analysis was performed using one-way ANOVA test. b Colony formation was measured by incubating infected cells in 12-well plates for 2 weeks. c Representative western blots of SLC13A3, SLC7A5, SLC3A2, FTH1, TfR1, and GPX4 in sgControl and sgSLC13A3 HepG2 and SNU398 cells (n = 3 independent experiments, two replicates per group). d Mouse study design. Mice were intravenously injected with AAV8-CRISPR/Cas9 sgControl or sgSlc13a3 virus. After two weeks, mice were subjected to hydrodynamic tail vein injection (HTVi) of c-Met/β-catenin plasmids or AKT/β-catenin plasmids to induce liver tumors. e Mice were euthanized when they developed a high burden of liver tumors (sgControl, gray curve; sgSlc13a3, blue curve). The log-rank test was used to compare overall survival between groups. f Gross images of liver tumors in mice with or without sgSlc13a3 injection. Images were representative shown out of 6 independent mice per group. g Representative images of H&E and IHC staining. Images were representative shown out of 6 independent mice per group. Scale bar, 200 μm. Source data are provided as a Source Data file.