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. 2017 Feb 1;8(11):17995–18009. doi: 10.18632/oncotarget.14929

Figure 6. Activation of ERK facilitates MYC suppression under drug induced stress conditions.

Figure 6

A. MYC expression in nuclear extracts from HCC366 cells transduced with GFP, mutant KRAS (G12D, G12C or G12V), PIK3CA H1047R (PIK3CAm), EGFRvIII (EGFRm), BRAF V600E (BRAFm), CRAF 22W (CRAFm) or RALA Q75L (RALAm). Cells were treated with BGT inhibitors at 0.1 μM or GC at 5 μM for 2 d. B. MYC expression in nuclear extracts from HCC366 cells transduced with GFP, KRAS G12D (KRASm), BRAF V600E (BRAFm), MEK1 C121S (MEK1m), ERK2 R67S D321N (ERK2m) or PIK3CA H1047R. Cells were treated with vehicle alone or GC at 5 μM for 2 d in the presence or absence of GSK1120212 (GC/G), BEZ235 plus GSK1120212 (GC/BG) and SCH772984 (GC/S) at 0.1 μM each. C. MYC mRNA expression in HCC366 cells transduced with vector alone or KRAS G12D-expressing retroviruses and treated with the indicated inhibitors for 2d. Relative levels of MYC mRNA were normalized to the expression HPRT mRNA. D. A proposed mechanism of MYC regulation by ERK and DNA damage response (DDR) signaling.