Fig. 4 | Nature Communications

Fig. 4

From: Survival of pancreatic cancer cells lacking KRAS function

Fig. 4

PI3K inhibition functions through AKT-dependent and -independent mechanisms. a Western blot showed stable pERK1/2 but increased pAKT and pPRAS40 levels in 8988T and A13 KRAS deficient (purple) cells, consistent with PI3K/AKT pathway activation. HSP90 is loading control. b Dose-response curves of 8988T and A13 KRAS intact (gray) and deficient (purples) clones to the pan-AKT inhibitor MK2206. Each replicate (n = 3 for each dose) and curve fit are shown. c Western blot showed sustained phosphorylation of AKT and downstream targets (PRAS40, S6, and 4EBP1) only in myr-AKT1- and myr-AKT2-expressing cells but not in myr-AKT1 (K179M)- or control GFP-expressing cells following 4 h of 2 μM GDC-0941 treatment. d Dose-response curves of cell lines in c treated with GDC-0941 and BAY80-6946 demonstrated a marked decrease in PI3K sensitivity with myr-AKT1 or myr-AKT2 overexpression. Each replicate (n = 3 for each dose) and curve fit are shown

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