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• W2015691830 abstract "The actin filament–associated protein AFAP-110 is an actin cross-linking protein first identified as a substrate of the viral oncogene v-Src. AFAP-110 regulates actin cytoskeleton integrity but also functions as an adaptor protein that affects crosstalk between Src and PKC. Here we investigated the roles of AFAP-110 in the tumorigenic process of prostate carcinoma. Using immunohistochemistry of human tissue arrays, we found that AFAP-110 was absent or expressed at very low levels in normal prostatic epithelium and benign prostatic hyperplasia but significantly increased in prostate carcinomas. The level of AFAP-110 in carcinomas correlated with the Gleason scores. Downregulation of AFAP-110 in PC3 prostate cancer cells inhibited cell proliferation in vitro and tumorigenicity and growth in orthotopic nude mouse models. Furthermore, downmodulation of AFAP-110 resulted in decreased cell-matrix adhesion and cell migration, defective focal adhesions, and reduced integrin β1 expression. Reintroduction of avian AFAP-110 or a mutant disabling its interaction with Src restored these properties. However, expression of an AFAP-110 lacking the PKC-interacting domain failed to restore properties of parental cells. Thus, increased expression of AFAP-110 is associated with progressive stages of prostate cancer and is critical for tumorigenic growth, in part by regulating focal contacts in a PKC-dependent mechanism." @default.
• W2015691830 created "2016-06-24" @default.
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• W2015691830 date "2007-10-01" @default.
• W2015691830 modified "2023-09-30" @default.
• W2015691830 title "AFAP-110 is overexpressed in prostate cancer and contributes to tumorigenic growth by regulating focal contacts" @default.
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• W2015691830 doi "https://doi.org/10.1172/jci30710" @default.
• W2015691830 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1978423" @default.
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