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Epigenetic repression of ROR2 has a Wnt-mediated, pro-tumourigenic role in colon cancer

Ester Lara1, Vincenzo Calvanese, Covadonga Huidobro

  • 1Department of Immunology and Oncology, National Center for Biotechnology, CNB-CSIC, Cantoblanco, Madrid E-28049, Spain.

Molecular Cancer
|July 2, 2010
PubMed
Abstract

Insights

Aberrant methylation of ROR2, a non-canonical Wnt pathway receptor, is frequent in colon cancer. Its loss promotes tumors by impacting canonical Wnt signaling, revealing a crucial link between Wnt pathways in cancer.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • Wnt signaling pathways, canonical (beta-catenin-dependent) and non-canonical (beta-catenin-independent), regulate cell differentiation.
  • Alterations in canonical Wnt signaling are key drivers of colon cancer.
  • The role of non-canonical Wnt pathways in tumorigenesis is not well understood.

Purpose of the Study:

  • Investigate the role of the non-canonical Wnt receptor ROR2 in colon cancer.
  • Determine the mechanisms of ROR2 regulation in colon cancer.
  • Explore the interplay between canonical and non-canonical Wnt pathways in colon cancer.

Main Methods:

  • Analysis of ROR2 promoter methylation in colon cancer cell lines and primary tumors.
  • Restoration of ROR2 activity in colon cancer cells.
  • Assessment of Wnt pathway activation following ROR2 restoration.

Main Results:

  • ROR2 is frequently repressed by promoter hypermethylation in colon cancer.
  • Restoring ROR2 activity in cancer cells impacts canonical Wnt signaling.
  • Epigenetic silencing of ROR2 is pro-tumorigenic in colon cancer.

Conclusions:

  • Epigenetic repression of ROR2 is a significant event in colon cancer.
  • ROR2's function in colon cancer involves canonical Wnt signaling.
  • This study highlights the interconnection between canonical and non-canonical Wnt pathways in colon cancer.

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