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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 2. Suppression of the FAS-NF-κB pathway enhances EGFR TKI response in EGFR-mutant cells and tumour models.

Figure 2

a, Erlotinib dose response in H1650 cells expressing a non-target control shRNA or a FAS (shRNA2), RELA (shRNA1), or c-FLIP(shRNA1) shRNA (5 μM erlotinib IC50 in parental H1650 cells). Cell viability was assayed as in Fig. 1. n = 3; mean + s.e.m. b, Immunoblots showing expression of indicated signalling proteins in H1650 cells generated in a. Data represent three independent experiments. NT, non-target; PARPcl, PARP cleaved. (The decrease in c-FLIP protein by shRNA was less complete than the decrease in c-FLIP mRNA level by siRNA; Supplementary Fig. 1). c, Effects of stable knockdown of FAS (shRNA3) or RELA (shRNA2) on erlotinib sensitivity in H1650 xenograft tumours, compared to non-target shRNA control H1650 tumours. Established tumours (>200 mm3,, n = 10 per treatment group) were randomized and treated for 7 days with 12.5 mg erlotinib per kg per day, n = 10. Data expressed as mean + s.e.m. d, Immunoblots showing expression of indicated proteins in representative H1650 tumour xenografts from c analysed at treatment day 7.