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    BIOMARKER:

    S100A16 overexpression

    i
    Other names: S100A16, S10000 Calcium Binding Protein A16, S100F, Aging-Associated Gene 13 Protein, Protein S100-A16, Protein S100-F, S100 Calcium-Binding Protein A16, Aging-Associated Protein 13, AAG13
    Entrez ID:
    140576
    2years
    LncRNA PRKCA-AS1 promotes LUAD progression and function as a ceRNA to regulate S100A16 by sponging miR-508-5p. (PubMed, J Cancer)
    Moreover, rescue experiment and tumorigenesis experiment in nude mice further confirmed that LncRNA PRKCA-AS1 regulates S100A16 through sponging miR-508-5p to regulate LUAD progression in vitro and in vivo. These results demonstrated that LncRNA PRKCA-AS1 might regulate LUAD by acting as a ceRNA via sponging miR-508-5p and regulating S100A16 expression, indicating that manipulation of PRKCA-AS1 might be a potential therapeutic strategy in LUAD.
    Journal
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    MIR508 (MicroRNA 508) • PRKCA (Protein Kinase C Alpha) • S100A16 (S100 Calcium Binding Protein A16)
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    S100A16 overexpression
    almost3years
    S100 Calcium Binding Protein A16 Promotes Cell Proliferation by triggering LATS1 ubiquitin degradation mediated by CUL4A ligase to inhibit Hippo pathway in Glioma development. (PubMed, Int J Biol Sci)
    This study demonstrated a vital biological role of S100A16 in glioma progression mechanism by promoting CUL4A-mediated LATS1 ubiquitination to inhibit Hippo signaling pathway. S100A16 could be a novel biomarker and treatment option for glioma patients.
    Journal
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    CUL4A (Cullin 4A) • LATS1 (Large Tumor Suppressor Kinase 1) • S100A16 (S100 Calcium Binding Protein A16) • CCN1 (Cellular Communication Network Factor 1) • CTGF (Connective tissue growth factor)
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    S100A16 overexpression
    over4years
    Calcium Binding Protein S100A16 Expedites Proliferation, Invasion and Epithelial-Mesenchymal Transition Process in Gastric Cancer. (PubMed, Front Cell Dev Biol)
    Mechanistic assay results indicate that excessive S100A16 instigates GC cell invasion, migration, and epithelial-mesenchymal transition (EMT) via ZO-2 inhibition, which arose from S100A16-mediated ZO-2 ubiquitination and degradation. Our results not only reveal that S100A16 is a promising candidate biomarker in GC early diagnosis and prediction of metastasis, but also establish the therapeutic importance of targeting S100A16 to prevent ZO-2 loss and suppress GC metastasis and progression.
    Journal
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    S100A16 (S100 Calcium Binding Protein A16)
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    S100A16 overexpression