Fig. 5: Treatment with TKI induces APOBEC3B upregulation.
From: The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance
a, GSEA of the indicated GEO2R datasets of EGFR-driven cellular models of human lung adenocarcinoma treated with erlotinib or a mitogen-activated protein kinase kinase (MAP2K or MEK1) inhibitor (AZD6244). b, RNA-seq analysis of gene expression changes in PC9 cells treated with 2 μM Osi for 9 d relative to DMSO-treated cells (n = 3 biological replicates, mean ± s.d., ANOVA test). c, RT–qPCR analysis of PC9 cells treated with DMSO or 2 μM Osi for 18 h (n = 4 biological replicates, mean ± s.d., one-way ANOVA test, *P = 0.0349, ****P < 0.0001). d, RT–qPCR analysis of HCC827 cells treated with DMSO or 0.4 μM osimertinib for 18 h (n = 4 biological replicates, mean ± s.d., one-way ANOVA test, ***P = 0.0008, **P = 0.0014). e, Western blot analysis of cells treated in a and b (CYTO, cytoplasmic extracts; H3, histone H3; NUC, nuclear extracts) with quantification of A3B levels in PC9 cells (n = 3 biological replicates, mean ± s.d., one-way ANOVA test, **P = 0.0012, **P = 0.0058) and HCC827 cells (n = 3 biological replicates, mean ± s.d., one-way ANOVA test, *P = 0.0186). f, RT–qPCR analysis of PC9 cells treated with nontargeting siRNA (siNTC) or EGFR siRNA (siEGFR) for 18 h and grown for 2 d (n = 4 biological replicates, mean ± s.d., two-sided t test, **P = 0.0075, ***P = 0.0002, **P = 0.0027). FC, fold change.
