Fig. 5: CT-induced quiescent cells display a fetal intestinal stem cell signature that is partially dependent on p53.

A Expression correlation matrix from the 28up + 8down-feISC gene signature in Marisa database (n = 566). Size of circles and color intensity are proportional to Pearson correlation coefficient for each gene pair. B RT-qPCR analysis of normalized expression of selected 28up + 8down-feISC genes in untreated and treated PDO5 (n = 2–4 biologically independent experiments). C WB analysis of control and 5-FU + Iri-treated PDO5 cells collected at the indicated time points (from one out of three biologically independent experiments). D–F RT-qPCR analysis of normalized relative expression of indicated genes in control and CT-treated TP53 WT PDO66 D, TP53 mutant PDO4 E and PDO5 TP53 KO #3 F (n = 2–4 biologically independent experiments). G WB analysis of PDO5 and PDO5 TP53 KO untreated or treated with 5-FU + Iri. at the same concentration at the indicated time points (from one out of three biologically independent experiments). H WB analysis with indicated antibodies of CRC cells untreated or treated 72 h with 5-FU + Iri. (from one out of three biologically independent experiments). I Pie charts showing the molecular subtype distribution according to Guinney et al., in patients within the feISC signature groups as indicated. J Distribution of selected 28up-fetal-ISC genes in epithelial subtypes cell states 1–9 described by Lee et al.³⁶. The t-SNE plots were obtained using the web-based tool URECA (User-friendly InteRface tool to Explore Cell Atlas). For all applicable figure panels, data are mean ± SD. Significance (p) was calculated with a two-sided Student’s t test. *p < 0.05; **p < 0.01; ****p < 0.0001; n.s., no significant. CT, control; IC₂₀ and IC₃₀, 5-FU + Iri. treatment indicates 20 and 30% cell death, respectively. Source data are provided as a Source Data file.