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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 4. — PRL-3 promotes peritoneal spreading via the PI3K/AKT signaling pathway in vivo. (A) Representative peritoneal dissemination of SGC7901 cells in LY294002-treated mice. Mice were sacrificed 4 weeks post-injection and the peritoneum was observed. (B) The total number of metastatic nodules on the peritoneal surface in each treatment group. (C) The number of metastatic nodules >1 mm³ in each treatment group. The number of metastatic nodules was significantly lower in the high+LY group. The bars represent the mean ± standard deviation (n=6/group). *P<0.05 vs. the control group. Mock, normal nude mice; vector, SGC7901 transfected with control empty vector; high, SGC7901/EGFP-PRL-3 cells; high+LY, plasmid SGC7901/EGFP-PRL-3/LY294002 cells. PRL-3, phosphatase of regenerating liver-3; AKT, RAC serine/threonine-protein kinase; PI3K, phosphatidylinositol 3-kinase.