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• W2017010587 abstract "Abstract Ovarian cancer is a leading cause of cancer death in women, is usually diagnosed in late stage, and currently has insufficient effective targeted therapies. The primary mode of metastasis is unique in that dissemination occurs via tumor cell shedding into the peritoneal cavity, survival and growth within ascites, and re-adhesion and proliferation of tumor cells at sites within the abdomen. Therefore, molecules and pathways involving cell adhesion and survival in non-adherent environments are of particular interest. Rgnef (p190RhoGEF/Arhgef28) is a Rho family guanine exchange factor that associates with focal adhesion kinase (FAK) and functions both as a downstream target of FAK tyrosine kinase activity and a regulator of FAK activity following integrin stimulation. FAK regulates cell adhesion, migration, and survival. Expression of FAK is associated with poor clinical outcome, its activity (as measured by FAK Y397 phosphorylation) is frequently increased in serous ovarian carcinomas, and it is currently under investigation as a therapeutic target in ongoing clinical trials. Immunohistochemical analysis of human tumor tissue arrays with antibodies specific for Rgnef and FAK pY397 reveal a positive correlation between Rgnef expression and FAK activation and increased stage/grade of serous-type ovarian cancer. Stable knockdown of Rgnef in human ovarian carcinoma cells grown as subcutaneous or intraperitoneal xenografts in mice suggest that Rgnef may play roles in both primary tumor growth and ascites-associated cell survival and spread. Here, we use a transgenic model of spontaneous ovarian cancer (MISIIR-T-Antigen) to test the role of Rgnef in ovarian cancer progression. Female Rgnef+/+;TAg+ and Rgnef-/-;TAg+ mice were monitored by ultrasound imaging from age 12 to 17 weeks before euthanasia. Rgnef-/-;TAg+ tumors were significantly smaller (p=0.0006) and contained fewer Ki67 positive cells than Rgnef+/+;TAg+ controls at 17 weeks. Tumors and ovarian carcinoma cells isolated from Rgnef-/-;TAg+ mouse ascites have reduced FAK pY397 and increased E-cadherin expression compared to controls, suggesting that loss of Rgnef results in a less aggressive tumor phenotype. These findings identify Rgnef as a component in signaling pathways promoting FAK activation and regulating ovarian tumor progression. Citation Format: Nichol L. G. Miller, Isabelle Tancioni, Sean Uryu, Elizabeth G. Kleinschmidt, Denise C. Connolly, David D. Schlaepfer. An Rgnef (p190RhoGEF/Arhgef28) signaling axis regulates ovarian cancer progression. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3157. doi:10.1158/1538-7445.AM2014-3157" @default.
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• W2017010587 date "2014-10-01" @default.
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• W2017010587 title "Abstract 3157: An Rgnef (p190RhoGEF/Arhgef28) signaling axis regulates ovarian cancer progression" @default.
• W2017010587 doi "https://doi.org/10.1158/1538-7445.am2014-3157" @default.
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