Fig. 2: BCL-2 dependence is lost immediately after transformation.
From: BCL-XL is crucial for progression through the adenoma-to-carcinoma sequence of colorectal cancer
a, b Graphs depict relative outgrowth of human normal colon organoids a WT1 and b WT2 quantified 3 days after passaging, upon treatment with 1 µM ABT-199 or A-1155463. Each dot represents a replicate (minimal n = 9 per condition, n = 3 independent experiments), error bars indicate s.e.m. c, d Graphs depict relative outgrowth of human APCKO organoids quantified 3 days after passaging, upon treatment with indicated doses of c ABT-199 or d A-1155463. Each dot represents a replicate (minimal n = 9 per condition, n = 3 independent experiments), error bars indicate s.e.m. ****p < 0.0001, ordinary one-way ANOVA. e Cleaved caspase-3 stained human normal (WT) and APCKO organoids after 24 h treatment with 300 nM ABT-199 or A-1155463. Scale bars, 200 µm. f Images represent the outgrowth of APCKO organoids after transduction with either control or BCL-XL targeting shRNA. g Dose-response curve of control vector (black) or BCL-XL overexpressing (red) APCKO organoids treated with a titration of A-1155463. Viability data measured by cell titer blue was blank corrected and normalized to untreated control. Data were represented as mean ± SD (n = 2 independent experiments). h Relative outgrowth of human mutant organoids of indicated genotypes quantified 3 days after passaging, upon treatment with 3 µM of ABT-199 or A-1155463 (n = 3 independent experiments). Error bars indicate s.e.m. *p < 0.05, ***p < 0.001, ****p < 0.0001, ordinary one-way ANOVA.
