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The EPH receptor Bs (EPHBs) promoters are unmethylated in colon and ovarian cancers

Qinghua Wu1, Guro E Lind, Hans-Christian Aasheim

  • 1Department of Pathology, Rikshospitalet-Radiumhospitalet Medical Center, University of Oslo, Oslo, Norway.

Epigenetics
|February 19, 2008
PubMed

Insights

Promoter hypermethylation is not a common cause of EPHB2, EPHB3, and EPHB4 gene silencing in colon and ovarian cancers. These EPHB family members do not appear to play a major role in these tumor types.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Aberrant EPH receptor and ephrin expression is observed in various human cancers.
  • Previous studies noted decreased EPHB expression in colorectal carcinomas, suggesting potential epigenetic regulation.

Purpose of the Study:

  • To investigate the promoter methylation status of EPHB2, EPHB3, and EPHB4 in colon and ovarian cancer.
  • To determine if promoter hypermethylation contributes to the altered expression of these EPHB family members in cancer.

Main Methods:

  • Analysis of promoter methylation using methylation-specific polymerase chain reaction (MSP) and direct bisulphite sequencing.
  • Assessment of gene expression via reverse transcription polymerase chain reaction (RT-PCR) and Northern blotting.

Main Results:

  • The promoters of EPHB2, EPHB3, and EPHB4 were predominantly unmethylated across tested colon and ovarian cancer cell lines and tumor samples.
  • EPHB2 RNA expression showed minimal variation in ovarian cancer samples.

Conclusions:

  • Promoter hypermethylation is not a frequent event for EPHB2, EPHB3, and EPHB4 in colon and ovarian cancers.
  • Epigenetic silencing via promoter methylation does not appear to be a major mechanism driving EPHB family gene alterations in these cancers.

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