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. 2016 Mar 8;7(16):21799–21811. doi: 10.18632/oncotarget.7985

Figure 6. The inhibitory effect of PRL-3 on the AKT-GSK3β pathway and SRC and ERK1/2 activation.

Figure 6

(A) Reduction of the phosphorylation of AKT and GSK3β by PRL-3. Cell lysates were analyzed by Western blot analysis with antibodies against pAKT473, AKT1/2/3, pGSKβ9, GSKβ, and the c-myc tag. GAPDH was used as an internal control. (B) Reduction of SRC activation and ERK1/2 phosphorylation by PRL-3. The expression levels of pERK42/44, ERK1/2, pSRC416, SRC, and myc-tagged PRL-3 in wild-type and mutant PRL-3 stable clones were detected by Western blotting. β-actin was used as a loading control. (C) Suppression of SRC phosphorylation in A549 cells by PRL-3. Cell lysates from A549 cells transiently expressing wild-type and mutant alleles of PRL-3 were analyzed by Western blot analysis with anti-pSRC416, anti-pSRC527, anti-SRC, and anti-EGFP. β-actin was used as a loading control.