Fig. 5: UBE2S enhanced colorectal cancer development.

a Dox-induced UBE2S elevation activated the downstream targets of β-CATENIN. Relevant band intensities from western blot were measured by MultiGauge software (Fujifilm), and numbers were further determined by normalizing β-TUBULIN band intensity to MYC and CCND1 band intensity, respectively. b UBE2S elevation promoted proliferation of colorectal cancer cells. HCT116 cells expressing dox-inducible UBE2S were seeded into 6-well plate. The cell numbers were counted on the third day after dox treatment. The untreated cells HCT116 cells were used as controls. The level of ectopic UBE2S expression was monitored by western blot with the antibody against HA. c UBE2S knockdown inhibited proliferation of colorectal cancer cells. Two constructs expressing UBE2S shRNAs were transfected into HCT116 cells, respectively. The cell numbers were counted on the fourth day after transfection. Western blot with the antibody against UBE2S monitored the level of Ube2s. d The MTT assay was used to measure the proliferation of the UBE2S∆ HCT116 cells. e The colony formation assay was used to measure cell proliferation. The cells were stained with crystal violet (0.5% in 20% ethanol) for 10 min. f Xenograft mouse models quantitatively examined the tumor growth at multiple time points after injection of UBE2S∆−1 and control cells; t-test: ***p < 0.001; **p < 0.01; *p < 0.05. The data presented in a–e are based on three independent repeats. The number of mice for each group in f is seven