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. Author manuscript; available in PMC: 2013 Jan 10.
Published in final edited form as: Nature. 2011 Mar 24;471(7339):523–526. doi: 10.1038/nature09870

Figure 3. NF-κB activation through IκB downregulation confers EGFR TKI resistance in EGFR-mutant lung cancer models.

Figure 3

a, Correlation of IκB expression with EGFR TKI sensitivity in EGFR-mutant lung cancer cells (IκB mRNA expression from Oncomine; sensitive <0.02 μM IC50: HCC827, H3255, HCC4006; resistant >1 μM IC50: H1650, H1975, H820). b, Immunoblots showing IκB and pRELA expression in lysates from HCC827 treated with non-targeting or IκB siRNA pools. c, Viability (CellTiter-Glo assay) of HCC827 cells treated with non-target siRNA pool or IκB siRNA pool and either vehicle or erlotinib (100 nM). RLU is relative luciferase units (n = 3; mean + s.e.m.). d, e, Effects of stable knockdown of IκB on erlotinib sensitivity in HCC827 tumour xenografts compared to non-target shRNA control HCC827 tumours. Tumours were established and treated as in Fig. 2c (n = 8 per treatment group, mean + s.e.m., 7-day treatment). f, Immunoblots showing expression of indicated proteins in representative HCC827 tumour xenografts analysed at treatment day 7.