Fig. 6

APC mediates EHMT2's oncogenic functions in HCC. A Cell proliferation was determined by Ki67 staining. Hep3B and Huh1 cells were stably transfected with APC and treated with UNC0642 at a dose of 1.0 μM for 24 h. The nucleus of harvested cells was isolated. n = 6 (mean ± SD); n = 6 (mean ± SD); *p < 0.05 and ***p < 0.001 by student's t-test. B MTT assay determined the cell growth curve of Hep3B and Huh1 cells. Cells were treated with UNC0642 at a dose of 1.0 μM for 3 days. n = 6 (mean ± SD); *p < 0.05, **p < 0.01 and ***p < 0.001 by two-way ANOVA followed by post hoc Bonferroni multiple comparisons. C Soft agar assay determined the anchorage-independent growth ability of Hep3B and Huh1 cells. APC-overexpressed Hep3B and Huh1 cells were treated with UNC0642 at a dose of 1.0 μM with an interval of 3 days. n = 6 (mean ± SD); *p < 0.05 and ***p < 0.001 by student's t-test. D Tumor growth curve of Hep3B xenograft assay. APC-overexpressed Hep3B cells in 6A were used. Animals were administrated treated with UNC0642 at a dose of 1 mg/kg body weight via intraperitoneal with an interval of 3 days. n = 6 (mean ± SD); *p < 0.05, **p < 0.01 and ***p < 0.001 by two-way ANOVA followed by post hoc Bonferroni multiple comparisons. E Final tumor weight of Hep3B xenograft assay in 6D. The bottom picture is a representative of final tumors. n = 6 (mean ± SD); *p < 0.05 and ***p < 0.001 by student's t-test. F A working model shows the roles of EHMT2 in the pathogenesis of HCC. β-cate, β-catenin