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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: PIM kinases inhibit AMPK activation and promote tumorigenicity by phosphorylating LKB1

Fig. 1

AMPK phosphorylation is enhanced by PIM inhibitors in an LKB1-dependent fashion. a PC3, Hela and MCF7 cells were treated for 24 h with DMSO (0.1%) or either DHPCC9 or AZD1208 pan-PIM inhibitor (10 μM in 0.1% DMSO) and subjected to Western blotting with antibodies against phospho-AMPK (Thr172), AMPK or LKB1. ACTB staining was used as a loading control. Shown in the graph are representative images together with graphs, where the relative levels of phosphorylated versus total AMPK were quantitated in comparison to DMSO-treated control samples (average values ± SD, n = 3). b Wild-type (WT) PC3 or MCF7 cells or their knock-out derivatives lacking LKB1 (LKB1KO) were treated for 24 h with DMSO or 10 μM DHPCC9, and subjected to Western blotting. Shown in the graphs are relative AMPK phosphorylation levels in comparison to DMSO-treated WT samples (average values ± SD, n = 3). c LKB1KO derivatives of PC3 or MCF7 cells were transiently transfected with FLAG or FLAG-LKB1 plasmids, treated for 24 h with DMSO or 10 μM DHPCC9, and subjected to Western blotting. Shown in the graphs are relative AMPK phosphorylation levels in comparison to DMSO-treated FLAG-transfected samples (average values ± SD, n = 3)

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