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PRL-3: a metastasis-associated phosphatase in search of a function

Cells Tissues Organs. 2007;185(1-3):232-6. doi: 10.1159/000101324.

Abstract

The molecular and cellular events involved in cancer progression and metastasis remain much less well-defined than those involved in oncogenesis, despite the fact that cell metastasis is the major factor in cancer mortality. Thus, the discovery that the expression of a protein tyrosine phosphatase, protein of regenerating liver-3 (PRL-3), is upregulated in colon cancer metastases provided an exciting indication that the altered regulation of specific protein tyrosine phosphorylation events and signaling pathways might characterize these metastatic cells and/or be key in promoting the tumor-to-metastasis transition in this, and perhaps other, cancers of epithelial origin. However, the cellular substrate(s) of PRL-3 has not been identified, and little is known of PRL-3-mediated cellular signaling pathways. This review illustrates the significance of PRL-3 in promoting metastasis and the importance of determining the endogenous role of PRL-3.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Movement / genetics
  • Cell Movement / physiology
  • Humans
  • Immediate-Early Proteins / genetics
  • Immediate-Early Proteins / metabolism*
  • Neoplasm Invasiveness / genetics
  • Neoplasm Invasiveness / pathology
  • Neoplasm Metastasis / genetics
  • Neoplasm Metastasis / pathology
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • Protein Tyrosine Phosphatases / genetics
  • Protein Tyrosine Phosphatases / metabolism*

Substances

  • Immediate-Early Proteins
  • Neoplasm Proteins
  • Ptp4a3 protein, mouse
  • PTP4A3 protein, human
  • Protein Tyrosine Phosphatases