KRASG12D- and BRAFV600E-induced survival in PDECs requires IGF1R signaling. KRASG12D- and BRAFV600E-induced survival in PDECs requires IGF1R signaling.

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KRASG12D- and BRAFV600E-induced survival in PDECs requires IGF1R signaling. KRASG12D- and BRAFV600E-induced survival in PDECs requires IGF1R signaling. A, viability of Ink4a/Arf, Trp53 double null PDECs expressing KRASG12D, BRAFV600E, SHH, or GFP treated with DMSO or AG1024, plus 100 μmol/L cycloheximide. *, P < 0.01 compared with DMSO-treated cells of identical genotype. B, viability of Ink4a/Arf null PDECs expressing KRASG12D, BRAFV600E, SHH, or GFP treated with DMSO or AG1024 plus UV irradiation as measured by trypan blue exclusion. White bars untreated cells, black bars UV-treated cells. Values are normalized such that viability of untreated cells is 1. Results are representative of at least 2 experiments. *, P < 0.01 compared with DMSO-treated cells of identical genotype. C, impact of IGF1R- and IR-targeting shRNAs on the viability of KRASG12D- and GFP-expressing Ink4a/Arf, Trp53 double null PDECs treated with 100 μmol/L cycloheximide. *, P < 0.05 compared with cells treated with control shRNA. D, viability of Ink4a/Arf, Trp53 null PDECs expressing KRASG12D, BRAFV600E, or GFP, as well as ectopic IGF2 (or GFP as a control), following treatment with 100 μmol/L cycloheximide and the indicated inhibitors. White bars vehicle-treated cells, black bars cycloheximide-treated cells. Values are normalized such that viability of untreated cells is 1. Results are representative of at least 2 experiments. *, P < 0.05 compared with GFP expressing cells treated with PD98059. All error bars, SD; DMSO, dimethyl sulfoxide. Victoria A. Appleman et al. Mol Cancer Res 2012;10:1228-1239 ©2012 by American Association for Cancer Research