Fig. 4

CEP89 amplification is associated with lower G0 arrest capacity. a Network illustrating CEP89 interactions with cell cycle genes (from GeneMania). The edge colour indicates the interaction type, with green representing genetic interactions, orange representing predicted interactions and purple indicating pathway interactions. The edge width illustrates the interaction weight. b CA20 scores are significantly increased in TCGA primary tumours containing a CEP89 amplification. c Pan-cancer relationship between CA20 and G0 arrest scores across the TCGA cohort. d Cox proportional hazards analysis estimates of the log hazards ratio for the impact of CEP89 expression on patient prognosis within individual cancer studies, after adjusting for tumour stage. Patients with high expression of CEP89 show significantly worse prognosis within ACC, LUSC, LIHC, KIRC and STAD, but significantly better prognosis within HNSC, PAAD and KIRP studies. e Western blot showing depletion of Cep89 protein 48 h after siRNA transfection of NCI-H1299 cells. Mock is lipofectamine only; NTC is non-targeting control siRNA. B-actin is used as a loading control. f Graphs show that Cep89 depletion in NCI-H1299 cells leads to a reduction in nuclear number and an increase in the fraction of G0 arrested cells, measured by an increase in the percentage of EdU negative (24 h EdU pulse) and Phospho-Ser 807/811 Rb negative cells. One-way ANOVA, *p < 0.05, **p < 0.01. Mean of n = 3