Skip to main content
. Author manuscript; available in PMC: 2020 Aug 8.
Published in final edited form as: Cell. 2019 Aug 8;178(4):807–819.e21. doi: 10.1016/j.cell.2019.07.031

Figure 2: Mutual exclusive activation of NRF2 and EGFR pathways in human cancers.

Figure 2:

A) Unbiased, pan-cancer analysis of mutations that are significantly related (co-occurring or mutual exclusive) with KEAP1 and NRF2 using the SELECT algorithm (see text and methods for details); B) Oncoprint showing mutual exclusive relation between NRF2/ KEAP1 and EGFR mutations in human cancers; C) Nuclear extracts from HepG2 cells treated with NRF2 inducer DLS (1 μM, 24 hours), EGF (10 ng/mL, 24 hours), TGFα (1 nM, 24 hours) or DMSO and probed with antibodies against NRF2 and lamin B; D) Nuclear (upper panel) and cytoplasmic extracts (lower panel) from H3255 (EGFRL858R) cells transduced with EGFR-specific shRNA or control and immunoblotted with indicated antibodies; E) Viability of isogenic H3255 cells transduced with sgRNAs targeting KEAP1 or LacZ (control) and treated with erlotinib; error bars represent SD from 3 replicates; F) Lysates from paired PC9 cells transduced with indicated sgRNA-Cas9 constructs and treated with DMSO or erlotinib (10 nM, 6 hours) probed with the indicated antibodies. (* indicates p-value < 0.05 by two-tailed student t test). See also Figure S2 and Table S2.