Fig. 7

PRIM1 promoted P53 degradation via up-regulating UBE2C in HCC cells. a the Spearman correlation of PRIM1 with UBE2C in TCGA and ICGC datasets. b MHCC97H and HepG2 were transfected with Kd-UBE2C or OE-UBE2C plasmids, respectively. c The proliferation of HCC cells was detected by CCK-8 assay. d The colony formation of HCC cells in each group. e The growth of the 3D spheres derived from MHCC97H in each group during day 1–5. f The MHCC97H-derived spheroids in different group treated with sorafenib. g The mRNA levels of UBE2C with PRIM1 knockdown or overexpression in MHCC97H or HepG2 cells. h The protein levels of UBE2C and P53 with PRIM1 depletion or overexpression in MHCC97H or HepG2 cells. i The protein levels of P53 signaling markers in MHCC97H or HepG2 cells transfected with different plasmids. j The proliferation of MHCC97H or HepG2 cells transfected with different plasmids was detected by CCK-8. k The colony formation of MHCC97H or HepG2 cells in each group. l The sensitivity of MHCC97H or HepG2 cells transfected with different plasmids to sorafenib treatment. **P < 0.01; *P < 0.05