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Protein tyrosine phosphatase receptor U (PTPRU) is required for glioma growth and motility

Zhichuan Zhu1, Yongjie Liu1, Kui Li1

  • 1School of Pharmacy, East China University of Science and Technology, Shanghai 200237, China, Department of Neurosurgery, Shanghai Neurosurgical Center, Huashan Hospital, Fudan University, Shanghai 200030, China and Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

Carcinogenesis
|May 31, 2014
PubMed

Insights

The protein tyrosine phosphatase receptor U (PTPRU) promotes glioma progression by affecting beta-catenin and focal adhesion signaling. Knockdown of PTPRU suppressed tumor growth and spread in preclinical models.

Area of Science:

  • Neuro-oncology
  • Molecular biology
  • Cancer research

Background:

  • The protein tyrosine phosphatase receptor U (PTPRU) typically inhibits cancer cell adhesion and proliferation.
  • Its role in glioma, a primary brain tumor, remains largely uncharacterized.

Purpose of the Study:

  • To investigate the function and expression of PTPRU and its isoforms in glioma.
  • To determine the impact of PTPRU on glioma cell behavior and tumor progression.

Main Methods:

  • Analysis of PTPRU expression in glioma tissues and cell lines.
  • Short hairpin RNA (shRNA) mediated knockdown of PTPRU in vitro and in vivo.
  • Assessment of cell proliferation, survival, invasion, migration, adhesion, and tube formation.
  • Evaluation of beta-catenin and c-Cbl phosphorylation and transcriptional activity.
  • Analysis of focal adhesion protein stability.

Main Results:

  • Non-full-length PTPRU isoforms, particularly nuclear-localized ones, are highly expressed in glioma and correlate with malignancy grade.
  • PTPRU knockdown inhibited glioma cell proliferation, survival, invasion, migration, adhesion, and vasculogenic tube formation in vitro.
  • PTPRU knockdown suppressed intracranial tumor progression in vivo.
  • PTPRU depletion reduced beta-catenin tyrosine phosphorylation and transcriptional activity, and increased c-Cbl tyrosine phosphorylation.
  • PTPRU knockdown led to destabilization of focal adhesion proteins.

Conclusions:

  • Endogenous PTPRU promotes glioma progression through its influence on beta-catenin and focal adhesion signaling pathways.
  • Targeting PTPRU may represent a novel therapeutic strategy for glioma.

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