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• W2184786348 abstract "AbstractTransforming growth factor (TGF)-β is both a suppressor and promoter of tumorigenesis; however, its contribution to early tumor suppression and staging remains largely unknown. In search of the mechanism of early tumor suppression, we focus on Smad4, a transducer of TGF-β signaling, and embryonic liver fodrin (ELF), a β-spectrin, in tumorigenesis by linking a major, dynamic scaffolding protein and a key signaling protein. ELF activates and modulates Smad4 activation of the TGF-β response to confer cell polarity, to maintain cell architecture, and to inhibit epithelial-to-mesenchymal transition. In human gastric tumor samples, a significant loss of ELF and reduction of Smad4 expression was recently found. An examination of elf +/−, Smad4+/−, and elf +/−/Smad4+/− mice revealed that disruption of ELF and Smad4 displayed a synergistic effect on tumor formation in terms of incidence and duration, suggesting a cooperative interaction between ELF and Smad4 leading to enhanced tumor suppression. This review examines our understanding of the significance of the interactions between ELF and Smad4, through regulation of the TGF-β signaling pathway and repression of tumor formation.Key WordsTGF-βELFSmad4knockout micetumorigenesis" @default.
• W2184786348 created "2016-06-24" @default.
• W2184786348 creator A5065439236 @default.
• W2184786348 creator A5088812559 @default.
• W2184786348 creator A5091703176 @default.
• W2184786348 date "2008-01-01" @default.
• W2184786348 modified "2023-09-28" @default.
• W2184786348 title "Interaction of Smad4 and Embryonic Liver Fodrin-β-spectrin in Hyperplasia, Neoplasia, and Tumor Suppression" @default.
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• W2184786348 doi "https://doi.org/10.1007/978-1-59745-292-2_6" @default.
• W2184786348 hasPublicationYear "2008" @default.
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