Author/Authors :
Wang، نويسنده , , Haihe and Vardy، نويسنده , , Leah A. and Tan، نويسنده , , Cheng Peow and Loo، نويسنده , , Jia Min and Guo، نويسنده , , Ke and Li، نويسنده , , Jie and Lim، نويسنده , , Seng Gee and Zhou، نويسنده , , Jianbiao and Chng، نويسنده , , Wee Joo and Ng، نويسنده , , Siok Bian and Li، نويسنده , , Hui Xiang and Zeng، نويسنده , , Qi، نويسنده ,
Abstract :
Summary
pression of phosphatase of regenerating liver (PRL)-3 is associated with the progression of diverse human cancers. We show that the overexpression of PRL-3 protein is not directly associated with its transcript levels, indicating the existence of an underlying posttranscriptional regulation. The 5′ untranslanted region (UTR) of PRL-3 mRNA possesses triple GCCCAG motifs capable of suppressing mRNA translation through interaction with PolyC-RNA-binding protein 1 (PCBP1), which retards PRL-3 mRNA transcript incorporation into polyribosomes. Overexpression of PCBP1 inhibits PRL-3 expression and inactivates AKT, whereas knockdown of PCBP1 causes upregulation of PRL-3 protein levels, activation of AKT, and promotion of tumorigenesis. An inverse correlation between protein levels of PRL-3 and PCBP1 in human primary cancers supports the clinical relevance.
