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. 2016 Jul 1;30(13):1542–1557. doi: 10.1101/gad.284166.116

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© 2016 Fan et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 7. — Loss of FER reduced metastasis of ovarian cancer cells via the peritoneal cavity. (A) Knockdown efficiency was confirmed by immunoblotting in both FER shRNA CAOV4 cell lines prior to intraperitoneal injection. (B–H) Mice were injected intraperitoneally with 5 × 10⁶ CAOV4 cells expressing either shCon (n = 6), FER sh1 (n = 7), or FER sh2 (n = 6). After 4 wk, necropsy procedures were performed, and the ability of CAOV4 cells to metastasize to surrounding tissue/organs, including the peritoneal wall (B), diaphragm (C), omentum (D), mesentery (E), ovary (F), stomach (G), and liver (H), were assessed. (I) Working model: In the absence of the ligand HGF, FER directly phosphorylated MET, GAB1, and possibly SHP2. This led to the activation of SHP2–MAPK and RAC1–PAK1 signaling downstream from MET to potentiate the motility and invasiveness of ovarian cancer cells.