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Tumor-derived extracellular mutations of PTPRT /PTPrho are defective in cell adhesion

Jianshi Yu1, Scott Becka, Peng Zhang

  • 1Department of Genetics and Case Comprehensive Cancer Center, Case Western Reserve University, Euclid Avenue, Cleveland, OH 44106, USA.

Molecular Cancer Research : MCR
|July 23, 2008
PubMed

Insights

Receptor protein tyrosine phosphatase T (PTPRT/PTPrho) mutations in cancer impair its cell-cell adhesion function. Loss of this function may drive tumor migration and metastasis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Receptor protein tyrosine phosphatase T (PTPRT/PTPrho) is frequently mutated in various human cancers.
  • Over half of these mutations occur in the extracellular domain, but their functional impact is unknown.

Purpose of the Study:

  • To investigate the function of the extracellular domain of PTPRT/PTPrho.
  • To determine the impact of tumor-derived mutations on PTPRT/PTPrho function.

Main Methods:

  • Cell aggregation assays were used to assess homophilic interaction of PTPRT/PTPrho.
  • Specific interactions with PTPmu were tested.
  • The effect of tumor-derived mutations on cell aggregation was evaluated.

Main Results:

  • The extracellular domain of PTPRT/PTPrho mediates specific homophilic cell-cell aggregation.
  • PTPRT/PTPrho does not interact with its homolog PTPmu.
  • Five tumor-derived mutations in the extracellular domains resulted in impaired cell aggregation, indicating loss-of-function.

Conclusions:

  • PTPRT/PTPrho plays a role in cell-cell adhesion.
  • Mutational inactivation of PTPRT/PTPrho may contribute to tumor progression, including migration and metastasis.

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