Fig. 6

Impact of G0 arrest on patient prognosis and treatment response. a Disease-specific survival based on proliferation/G0 arrest levels for patients from TCGA within 15 years of follow-up. Patients with increased levels of G0 arrest in primary tumours showed significantly better prognosis than patients with fast proliferating tumours. b–c Hazard ratio ranges illustrating the impact of different forms of G0 induction (b) and different tissues (c) on patient prognosis, after taking into account potential confounding factors. Values above 0 indicate significantly better prognosis when tumours contain high proportions of cells arrested in G0. d Change in G0 arrest scores inferred from bulk RNA-seq across breast, pancreatic, colorectal and skin cancer cells in response to treatment with the CDK4/6 inhibitor palbociclib, 5-FU or the BRAF inhibitor vemurafenib. e–f UMAP plot illustrating the response of the TP53-proficient RKO colorectal cancer cell line to various 5-FU doses and the corresponding proportions of cells predicted to be arrested/proliferating. Each dot is an individual cell, coloured according to its G0 arrest level. g–h The same as previous, but for the TP53-deficient SW480 cell line. i–j UMAP plot illustrating the response of individual PC9 NSCLC cells to the EGFR inhibitor erlotinib across several time points and the corresponding proportion of cells predicted to be arrested/proliferating. k Principal component analysis illustrating the superimposition of single-cell RNA-seq profiles (circles) of G0 arrested NSCLC cells before/after EGFR inhibition onto the bulk RNA-seq reference data (triangles) for MCF10A cells occupying various stress response states. l The proportion of NSCLC cells in k predicted to occupy different stress response states across several time points