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Dystroglycan function is a novel determinant of tumor growth and behavior in prostate cancer

A Mitchell1, G Mathew, T Jiang

  • 1Department of Biomedical Science, University of Sheffield, Sheffield, UK.

The Prostate
|September 22, 2012
PubMed
Abstract

Insights

Changes in dystroglycan, a cell adhesion molecule, impact prostate cancer growth and invasion. Loss of dystroglycan promotes anchorage-independent growth but hinders invasion, suggesting a complex role in metastasis.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Biochemistry

Background:

  • Dystroglycan is a cell adhesion molecule often altered in adenocarcinomas.
  • Mechanisms and consequences of dystroglycan loss in cancer are not well understood.

Purpose of the Study:

  • To investigate the impact of dystroglycan alterations on prostate cancer cell properties.
  • To analyze the effects of dystroglycan overexpression and depletion on cell growth, migration, and invasion.

Main Methods:

  • Utilized LNCaP, PC3, and DU145 prostate cancer cell lines.
  • Examined consequences of dystroglycan overexpression and RNAi depletion.
  • Assessed in vitro growth, migration, and invasion properties.

Main Results:

  • Observed cell density-dependent changes in β-dystroglycan, including proteolysis and mis-glycosylation.
  • Dystroglycan localization varied, with membrane localization in mesenchymal cells and nuclear presence in some.
  • Increased dystroglycan inhibited soft agar growth but promoted invasion; reduced levels did the opposite.

Conclusions:

  • Altered dystroglycan distribution and loss via proteolysis/glycosylation enhance anchorage-independent growth.
  • Dystroglycan re-expression may be necessary for prostate cancer cell invasion and metastasis.

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