Fig. 6: SMYD5 promotes HCC both ex vivo and in vivo.

a Left, anchorage-independent growth analyses using 3D soft agar assay of the control and SMYD5 KO1 Huh7 cells under indicated treatments; quantification of the 3D spheroid volumes of the results was shown in the right panel. b Tumor volume quantification for Huh7 xenografts in nude mice (n = 4 for each group). The control and SMYD5 KO1 Huh7 xenografts were both treated with PBS or Torin1 25 mg/kg daily. Data were represented as mean ± SEM. c Tumor volume quantification for SNU499 xenografts in NSG mice (n = 5 for each group). The control and SMYD5 KO1 SNU449 cells, and the SMYD5 KO1 SNU449 cells overexpressing WT or catalytically deficient (mut) SMYD5 were used. 25 mg/kg Torin1 was used for intraperitoneal injection daily for the indicated groups. Data were represented as mean ± SEM. d Tumor volume quantification of HCC PDX in NSG mice (n = 4 for each group) from different two HCC patients. The siRNA that dissolved in the PBS with DMSO or 500 nM Torin1 was used for intratumoral injection every three days. Data were represented as mean ± SEM. e Schematic illustrating the animal HCC model utilized in the generation of liver-specific Smyd5 deletion; Lower, experimental design to assess effects of SMYD5 ablation on development of HCC with advanced liver fibrosis. f Left two columns, representative gross images of liver pathology (arrows indicate tumor nodules). HE-stained sections and IHC staining with the indicated antibodies of tumors from control and SMYD5-depleted mice at 6 months of age (representative of n = 8 mice for each group). Scale bars: 5 mm (whole mount) and 100 µm (section). g Quantifications of liver/body weight ratio, tumor number, tumor size, and pH3 positive cells in control and SMYD5-depleted tumor samples used in Fig. 6f. Boxes: 25th to 75th percentile; whiskers: min to max; center line: median; n = 8 mice for each group.