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Fig. 5 | Cell Communication and Signaling

Fig. 5

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

Fig. 5

Lack of both LKB1 and PIM kinases impairs cell proliferation and tumor growth. a WT PC3 or MCF7 cells or their LKB1-deficient KO derivatives were grown overnight on 96-well plates, after which they were treated with DMSO or 10 μM DHPCC9, and their proliferation was followed for 5 days using the IncuCyte live cell imaging system. Shown are average percentages of confluence at indicated time-points (± SD of a representative experiment, n = 3). b Proliferation assays were performed with WT PC3 or MCF7 cells or their KO or TKO derivatives lacking LKB1 and/or all PIM kinases, respectively (n = 3). c Phospho-AMPK (Thr172) versus AMPK levels were measured from WT cells in comparison to cells lacking all PIM family members or LKB1 or both PIM and LKB1 in PC3 and MCF7 cells (average values ± SD, n = 3). d WT PC3 and MCF7 cells or their KO and/or TKO derivatives were grown for 7 days on the chorioallantoic membranes (CAM) of chick embryos. Shown are scatter plots of tumor mass at the end of the experiment. Numbers of the samples are listed at the bottom of the graphs. e PC3 cells and their LKB1KO derivatives were transiently transfected with His or His-PIM1 plasmids for 48 h before being grown for 7 days on CAM. Parts of the xenograft samples were subjected to Western blotting to examine PIM1 and LKB1 expression levels. Shown are scatter plots of tumor mass at the end of the experiment. Numbers of the samples are listed at the bottom of the graphs

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