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    BIOMARKER:

    DDX39B overexpression

    i
    Other names: DDX39B, DExD-Box Helicase 39B, UAP56, D6S81E, BAT1, DEAD (Asp-Glu-Ala-Asp) Box Polypeptide 39B, HLA-B-Associated Transcript 1 Protein, 56 KDa U2AF65-Associated Protein, Spliceosome RNA Helicase DDX39B, ATP-Dependent RNA Helicase P47, DEAD-Box Helicase 39B, Nuclear RNA Helicase (DEAD Family), HLA-B Associated Transcript 1, Spliceosome RNA Helicase BAT1, U2AF65-Associated Protein 56, DEAD Box Protein UAP56
    Entrez ID:
    7919
    3years
    HLA-BAT1 alters migration, invasion and pro-inflammatory cytokines in prostate cancer. (PubMed, Front Oncol)
    Our in vivo studies demonstrated up-regulation of TNF-α, IL-6, and MMP10 in tumors developed from transfected BAT1 shRNA cells when compared to tumors developed from BAT1 cDNA cells. These findings indicate that BAT1 down-regulation modulates TNF-α and IL-6 expression which may lead to the secretion of MMP-10 and inhibition of TIMP2.
    Journal
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    IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • HLA-B (Major Histocompatibility Complex, Class I, B) • TIMP2 (TIMP Metallopeptidase Inhibitor 2) • DDX39B (DExD-Box Helicase 39B)
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    DDX39B overexpression • IL6 expression
    over3years
    DDX39B drives colorectal cancer progression by promoting the stability and nuclear translocation of PKM2. (PubMed, Signal Transduct Target Ther)
    In addition, blocking PKM2 nuclear translocation or treatment with glycolytic inhibitor 2-deoxy-D-glucose efficiently abolishes DDX39B-triggered malignant development in CRC. Taken together, our findings uncover a key role for DDX39B in modulating glycolytic reprogramming and aggressive progression, and implicate DDX39B as a potential therapeutic target in CRC.
    Journal
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    DDX39B (DExD-Box Helicase 39B) • PKM (Pyruvate Kinase M1/2)
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    DDX39B overexpression