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The metastasis-associated gene Prl-3 is a p53 target involved in cell-cycle regulation

Shashwati Basak1, Suzanne B R Jacobs, Adam J Krieg

  • 1Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.

Molecular Cell
|May 13, 2008
PubMed

Insights

Prl-3, a gene induced by the tumor suppressor p53, acts as a crucial cell-cycle regulator. Its dual role in cell-cycle progression and cancer progression offers new therapeutic insights.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The p53 tumor suppressor is critical in preventing cancer by regulating genes for cell-cycle arrest and apoptosis.
  • Prl-3 (phosphatase of regenerating liver-3) has been linked to cancer metastasis due to its overexpression in colorectal cancer and promotion of cell invasiveness.

Purpose of the Study:

  • To identify Prl-3 as a p53-inducible gene.
  • To elucidate the role of Prl-3 in cell-cycle regulation and cancer progression, beyond its previously known role in metastasis.

Main Methods:

  • Identification of Prl-3 as a p53 target gene.
  • Investigation of Prl-3's function in cell-cycle regulation through overexpression and attenuation studies.
  • Analysis of signaling pathways involved, including PI3K-Akt.

Main Results:

  • Prl-3 is confirmed as a p53-inducible gene.
  • Prl-3 overexpression induces G1 cell-cycle arrest downstream of p53, mediated by a PI3K-Akt feedback loop.
  • Reduced Prl-3 expression also causes cell-cycle arrest, indicating its importance in normal cell-cycle progression.

Conclusions:

  • Prl-3 exhibits dose-dependent functions in regulating cell-cycle progression, acting as both a positive and negative regulator.
  • These findings reveal novel insights into Prl-3's multifaceted role in cancer development and progression.

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