Extended Data Fig. 8: JAK–STAT inhibitors have combined inhibitory effect on PCa cells with lineage plasticity.
a, IHC of the Trp53loxP/loxP, Rb1loxP/loxP + Empty (TP53/RB1-WT) and Trp53loxP/loxP, Rb1loxP/loxP + Cre (TP53/RB1-KO) organoids cultured in 3D, with annotated antibodies. b, IF of annotated organoids cultured in 3D, with annotated antibodies targeting canonical AR target genes and lineage marker genes. For panels a and b, representative pictures of n = 2 independent treated cell cultures were shown. c, Relative cell number of LNCaP/AR cells treated with annotated treatment: 10 µM enzalutamide (Enz), 5 µM filgotinib (Filg), 5 µM ruxolitinib (Ruxo), 1 µM fludarabine (Flu), 0.2 µM niclosamide (Nic) and DMSO for 8 days and cell numbers (viability) were measured using CellTiter-Glo assay, all normalized to vehicle group. p-values were calculated using one-way ANOVA with Bonferroni multiple-comparison test. d, Relative gene expression of JAK–STAT genes in xenograft-derived Enz resistant cell lines with CHD1-deficiency. e-g, Cell number of xenografted-derived Enz resistant cells upon treatment administration, measured by cell proliferation assay. For panels (e-g), Enz denotes 10 µM enzalutamide, Filg denotes 5 µM filgotinib, Rux denotes 5 µM ruxolitinib and Veh denotes DMSO treatment for 7 days. For all panels unless otherwise noted, n = 3 independently treated cell cultures and mean ± s.e.m. is represented. p-values were calculated using two-way ANOVA with Bonferroni multiple-comparison test and annotated in figures.
