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. 2018 Apr 11;15(6):9069–9074. doi: 10.3892/ol.2018.8467

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Copyright: © Zhang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — p-AKT, MMP-2 and MMP-9 are involved in PRL-3-mediated invasion and migration of gastric cancer cells. (A) Levels of PRL-3, AKT and p-AKT were analyzed in SGC7901 cells (control), SGC7901 cells transfected with empty vector, and plasmid SGC7901/EGFP-PRL-3 cells (high) by western blotting. (B) The expression of MMP-2 and MMP-9 were also analyzed by western blotting. (C) The relative expression of PRL-3 was quantified relative to β-actin. (D) The ratio of p-AKT/AKT was quantified relative to the control group. (E) The expression of MMP-2 was quantified relative to β-actin. (F) The expression of MMP-9 was quantified relative to β-actin. Each bar represents the mean ± standard deviation of 3 independent experiments. *P<0.05 vs. the control group. p-AKT, phosphorylated-RAC serine/threonine-protein kinase; MMP-2, matrix metallopeptidase-2; MMP-9, matrix metallopeptidase-9; PRL-3, phosphatase of regenerating liver-3; DMSO, dimethyl sulfoxide.