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Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
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Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

Published on: September 18, 2020

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Van-Gogh-like 2 antagonises the canonical WNT pathway and is methylated in colorectal cancers

G Piazzi1, M Selgrad, M Garcia

  • 1Department of Internal Medicine, Baylor Research Institute and Sammons Cancer Center, Baylor University Medical Center, 3500 Gaston Avenue, Dallas, TX 75246, USA.

British Journal of Cancer
|April 13, 2013
PubMed
Abstract

Insights

Van-Gogh-like 2 (VANGL2) is often methylated in colorectal cancer (CRC) with specific mutations. VANGL2 may suppress tumors by inhibiting WNT/β-catenin signaling, offering a potential therapeutic target for CRC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Aberrant WNT signaling is a hallmark of colorectal cancer (CRC).
  • Van-Gogh-like 2 (VANGL2), part of the non-canonical WNT pathway, inhibits canonical WNT signaling.
  • Investigating VANGL2's role and epigenetic regulation in CRC is crucial.

Purpose of the Study:

  • To investigate the role of Van-Gogh-like 2 (VANGL2) in colorectal cancer (CRC).
  • To explore the epigenetic regulation of VANGL2 in CRC.
  • To determine VANGL2's potential as a tumor suppressor gene.

Main Methods:

  • Assessed VANGL2 expression and promoter methylation in CRC cells after 5-aza-2'-deoxycytidine treatment.
  • Analyzed VANGL2 promoter methylation and microsatellite instability (MSI) in 418 sporadic CRC specimens.
  • Evaluated proliferation, colony formation, and WNT pathway activation following VANGL2 overexpression.

Main Results:

  • VANGL2 mRNA increased in 5-aza-treated CRC cells; methylation varied across cell lines, correlating with expression levels.
  • In CRC specimens, methylated VANGL2 was linked to MSI, higher grade, proximal location, and BRAF mutation.
  • Overexpression of VANGL2 in SW480 cells reduced proliferation, colony formation, and β-catenin levels.

Conclusions:

  • VANGL2 is frequently methylated in MSI-CRCs with BRAF mutations.
  • VANGL2 functions as a tumor suppressor gene by counteracting WNT/β-catenin signaling.
  • Epigenetic silencing of VANGL2 may contribute to CRC development.

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