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    BIOMARKER:

    PTP4A3 overexpression

    i
    Other names: PTP4A3, Protein Tyrosine Phosphatase 4A3, Protein-Tyrosine Phosphatase Of Regenerating Liver 3, Protein Tyrosine Phosphatase Type IVA, Member 3, Protein Tyrosine Phosphatase Type IVA 3, Phosphatase Of Regenerating Liver 3, PRL-3, PRL-R, PRL3, Potentially Prenylated Protein Tyrosine Phosphatase, Protein-Tyrosine Phosphatase 4a3
    Entrez ID:
    11156
    over3years
    The Deubiquitinating Enzyme USP4 Functions as an Oncoprotein in Gastric Cancer and Mediates NF-κB Signaling by Regulating PRL-3 Expression. (PubMed, Front Biosci (Landmark Ed))
    This study indicated that elevated USP4 predicted a poor index for gastric cancer patients, and mediated gastric cancer cell growth by regulating PRL-3/NF-κB signaling, which suggested USP4 may be a novel therapeutic target for gastric cancer.
    Journal • IO biomarker
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    BCL2 (B-cell CLL/lymphoma 2) • CCND2 (Cyclin D2) • PTP4A3 (Protein Tyrosine Phosphatase 4A3)
    |
    PTP4A3 overexpression
    almost4years
    The phosphatase of regenerating liver-3 protein(PRL-3)promotes glioma cell invasiveness by interacting with β3 -tubulin. (PubMed, Bioengineered)
    Taken together , our study revealed that PRL-3 may be involved in migration and invasion of glioma by dephosphorylating β3-tubulin. It is tempting to speculate that dephosphorylation of β3-tubulin by PRL-3 results in assembly of the cytoskeleton and facilitate the cell migration and/or tumor metastasis.
    Journal
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    PTP4A3 (Protein Tyrosine Phosphatase 4A3)
    |
    PTP4A3 overexpression
    over5years
    PRL-3 facilitates Hepatocellular Carcinoma progression by co-amplifying with and activating FAK. (PubMed, Theranostics)
    Furthermore, the p38 and PI3K/AKT pathways were observed to mediate the PRL-3-induced expression of TGFB1 and the subsequent activation of FAK, while the activation of FAK in turn stimulated activation of the p38 and PI3K/AKT pathways, forming a PRL-3-triggered AKT/p38/TGFB1/FAK positive feedback loop. Collectively, our findings indicate that the PTP PRL-3 plays a crucial role in the progression of HCC and provides an example of how co-amplified genes work together in HCC.
    Journal
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    TGFB1 (Transforming Growth Factor Beta 1) • PTP4A3 (Protein Tyrosine Phosphatase 4A3)
    |
    PTP4A3 overexpression