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. Author manuscript; available in PMC: 2015 Aug 31.
Published in final edited form as: Oncogene. 2011 Jul 18;31(7):818–827. doi: 10.1038/onc.2011.281

Figure 6. Both catalytic activity and C-terminal CAAX domain were critical for PRL-2 function.

Figure 6

A) A549 cells were transfected with HA control, HA-PRL-2, the catalytic dead mutant C101S or ΔCAAX deletion mutant. After 16 h, cells that migrate to the lower chamber were fixed, stained, and counted with a microscope. Percent cell migration was determined by normalizing the number of migrated cells in the HA-PRL-2 wells to HA vector controls. The mean values of three independent experiments measured in triplicate are show; bars equal SEM. *, p<0.01. B) Cells were plated on Matrigel matrix and after 24 h, cells that invade to the lower chamber were fixed, stained, and counted as above. N=3; bars = SEM. *, p<0.01. C) Increased pERK after expression of wild type HA-PRL-2 but not the mutants. A549 cells were transfected with HA control, HA-PRL-2, the catalytic dead mutant C101S or ΔCAAX deletion mutant. Cells were harvested 24 h later for Western blotting. Average fold changes from three independent experiments normalized to HA vector control cells were shown above the Western blots. D) Western blotting confirmed the over-expression of HA-PRL-2 and its mutants.