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PCBP1 suppresses the translation of metastasis-associated PRL-3 phosphatase

Haihe Wang1, Leah A Vardy, Cheng Peow Tan

  • 1Institute of Molecular and Cell Biology, A*Agency for Science, Technology and Research, 61 Biopolis Drive, Proteos, Singapore 138648, Republic of Singapore.

Cancer Cell
|July 9, 2010
PubMed

Insights

Phosphatase of regenerating liver (PRL)-3 protein levels are regulated post-transcriptionally by PolyC-RNA-binding protein 1 (PCBP1) through its 5' untranslated region. This interaction impacts cancer progression and AKT signaling.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Post-transcriptional Regulation

Background:

  • Overexpression of phosphatase of regenerating liver (PRL)-3 is linked to human cancer progression.
  • PRL-3 protein levels do not directly correlate with its mRNA transcript levels, suggesting post-transcriptional control.

Purpose of the Study:

  • To investigate the post-transcriptional mechanisms regulating PRL-3 expression.
  • To identify the role of PolyC-RNA-binding protein 1 (PCBP1) in PRL-3 regulation and its impact on cancer pathways.

Main Methods:

  • Analysis of 5' untranslated region (UTR) of PRL-3 mRNA for regulatory elements.
  • Investigating the interaction between PRL-3 mRNA and PCBP1.
  • Assessing the effects of PCBP1 overexpression and knockdown on PRL-3 protein levels, AKT signaling, and tumorigenesis.
  • Correlating PRL-3 and PCBP1 protein levels in human cancer tissues.

Main Results:

  • The 5' UTR of PRL-3 mRNA contains triple GCCCAG motifs that bind PCBP1, suppressing translation.
  • PCBP1 overexpression inhibits PRL-3 expression and inactivates AKT.
  • PCBP1 knockdown leads to increased PRL-3 protein, AKT activation, and promotes tumorigenesis.
  • An inverse correlation between PRL-3 and PCBP1 protein levels was observed in human primary cancers.

Conclusions:

  • PCBP1 acts as a negative regulator of PRL-3 expression via post-transcriptional mechanisms involving the 5' UTR.
  • The PRL-3/PCBP1 axis influences AKT signaling and tumorigenesis, highlighting its clinical relevance in human cancers.

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