Fig. 2

EGR1 downregulation prompted HCC cells proliferation in vitro and facilitated tumor growth in vivo. A We performed WB assays to evaluate the presence of EGR1 in normal liver cell line and HCC cell lines. B The protein expression of EGR1 was observed in MHCC97H and HCCLM3 cells following the knockout or silencing of EGR1 using WB assays. C The IncuCyte zoom cell proliferation assays were used to assess the effect of EGR1 knockout or silencing on the growth of HCC cells. D To validate the influence of EGR1 knockout or silencing on the growth of HCC cells, EDU incorporation assays were performed. E The ability of HCC cells to form colonies was evaluated by conducting colony formation assays following the knockout or silencing of EGR1. F Xenograft tumor assays were conducted on parental and EGR1 knockout MHCC97H cells in order to examine the impact of EGR1 knockout on the growth of xenograft tumors. Tumor volume was assessed at three-day intervals, and after 21 days, the tumors were gathered and measured in terms of weight. G Ki67 staining of the xenograft tumors was employed to validate the influence of EGR1 knockout on the growth of xenograft tumors. **P < 0.01, ***P < 0.001, ****P < 0.0001