کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2107715 | 1083696 | 2010 | 11 صفحه PDF | دانلود رایگان |
SummaryOverexpression 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.
► PRL-3 protein is upregulated in diverse human cancers
► PCBP1 suppresses PRL-3 translation via the 5′ UTR of the PRL-3 mRNA
► PCBP1 and PRL-3 protein levels were inversely correlated in human cancers
► The axis of PCBP1→PRL-3→AKT pathway in cancer cell signaling
Journal: - Volume 18, Issue 1, 13 July 2010, Pages 52–62