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  • Title: PRL-3 activates NF-κB signaling pathway by interacting with RAP1.
    Author: Lian S, Meng L, Liu C, Xing X, Song Q, Dong B, Han Y, Yang Y, Peng L, Qu L, Shou C.
    Journal: Biochem Biophys Res Commun; 2013 Jan 04; 430(1):196-201. PubMed ID: 23178297.
    Abstract:
    Phosphatase of regenerating liver (PRL-3) promotes cancer metastasis through enhanced cell motility and invasiveness, however its role in tumorigenesis remains unclear. Herein, we reported that PRL-3 interacts with telomere-related protein RAP1. PRL-3 promotes the cytosolic localization of RAP1, which is counteracted by silencing of PRL-3. Immunohistochemical staining of colon cancer tissue array (n=170) revealed that high level of PRL-3 associates with cytosolic localization of RAP1 (p=0.01). Microarray analysis showed that PRL-3 regulates expression of diverse genes and enhances phosphorylation of p65 subunit of NF-κB in a RAP1-dependent manner. Furthermore, PRL-3 transcriptionally activates RAP1 expression, which is counteracted by ablating p65. Therefore, our results demonstrate PRL-3 as a novel regulator of NF-κB signaling pathway through RAP1.
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