Fig. 4
From: Overexpression of Cullin7 is associated with hepatocellular carcinoma progression and pathogenesis
Knockdown of Cullin7 inhibited the proliferation, migration, and invasion capacities of HCC cells. a Knockdown of Cullin7 in specific shRNA-transduced stable HepG2 cells. Ī²-actin was used as a loading control. b The transfection efficiency of shCullin7 was analyzed by measuring transcript levels using qRT-PCR analyses in HepG2 cells. c Silencing endogenous Cullin7 inhibited cell growth as determined using MTT assays. d Silencing endogenous Cullin7 inhibited cell growth as determined using colony formation assays. Summary graphs are presented for the colony formation assay that is outlined. e HepG2 shCullin7 and control vector cells were subjected to a wound healing assay (left panels). The uncovered areas in the wound healing assays were quantified as a percentage of the original wound area. f HepG2 shCullin7 and control vector cells were subjected to Transwell migration (upper panels) and Matrigel invasion assays (lower panels). Quantification of migrated cells through the membrane and invaded cells through Matrigel of each cell line are shown as a proportion of the vector controls. Error bars represent the meanāĀ±āSD of three independent experiments