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Stable overexpression of AJAP1 promotes adherence, decreases invasion of glioma cells through an extracellular-like matrix, and slows migration in the presence of laminin. These observations are reversed by gene knockdown using multiple siRNAs. Additionally, overexpression of AJAP1 decreases colony formation in glioma cells.
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AJAP1 blocked epithelial-to-mesenchymal transition by interacting with beta-catenin and inhibiting its nuclear translocation, which suppressed zinc finger E-box binding homeobox 1 (ZEB1) transcription.
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EGFR/EGFRvIII remodels the cytoskeleton via epigenetic silencing of AJAP1 in glioma cells.
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Reduced Expression of Adherens Junctions Associated Protein 1 is associated with Recurrence of Hepatocellular Carcinoma After Curative Hepatectomy.
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These findings indicate that downregulated AJAP1 transcription may serve as a novel tumor biomarker to predict recurrence of ESCC after esophagectomy.
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Article summarizes and discusses current knowledge that may identify AJAP1 as a tumor suppressor in gliomas. [Review]
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Results show that AJAP1 is dysregulated at an early stage of gliomagenesis and may suppress glioma cell invasion and proliferation, which suggests that AJAP1 may be a potential diagnostic and prognostic marker for gliomas
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AJAP1 suppressed the expression of MAGEA2 and inhibited the transcriptional activity of MAGEA2 in glioma cells.
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We also identified a significant genetic association between caries of the mid- dentition tooth surfaces and AJAP1 (p value = 2e-8), a gene possibly involved in tooth development.
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This work shows the significant loss of expression of AJAP1 in glioblastoma and provides evidence of its role in the highly migratory characteristic of these tumors.
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Both genetic (gene deletion) and epigenetic alterations (promoter methylation) are likely mechanisms that inactivate the putative tumor suppressor AJAP1 in gliomas, which contributes to poor prognosis.
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Data show that overexpression of shrew-1 leads to preformation of an E-cadherin/EGF receptor/HER2/src-kinase/shrew-1 signaling complex and accelerated E-cadherin internalization.
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While a mutation was not detected in the coding region of the SHREW1 gene in oligodendrogliomas, SHREW1 expression restoration resulted in suppression of cell adhesion and migration, thus, SHREW1 inactivation may lead to oligodendroglial tumorigenesis.
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Adaptor protein complex AP-1B is involved in retaining shrew-1 at the basolateral membrane by postendocytic sorting mechanisms.
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shrew-1 has a function in the regulation of cellular invasion, which may involve its interaction with CD147
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synergism between a signal peptide and a transmembrane segment to mediate plasma membrane localization is essential for structural and/or functional integrity of shrew-1
