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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

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CD80 down-regulation is associated to aberrant DNA methylation in non-inflammatory colon carcinogenesis

Marco Scarpa1, Melania Scarpa2, Ignazio Castagliuolo3

  • 1Esophageal and Digestive Tract Surgery Unit, Veneto Institute of Oncology IOV - IRCCS, Padova, Italy. marcoscarpa73@yahoo.it.

BMC Cancer
|July 6, 2016
PubMed
Abstract

Insights

Genomic methylation, a key factor in cancer development, silences genes and reduces CD80 expression in colon carcinogenesis. Inhibiting DNA methylation restored CD80 levels, suggesting a link between methylation and immune evasion in colon cancer.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Tumor cells evade immune surveillance partly by lacking positive costimulatory molecules.
  • Promoter hypermethylation is a critical mechanism in cancer development, causing transcriptional silencing of genes.
  • Non-inflammatory colon carcinogenesis involves complex molecular alterations impacting immune response.

Purpose of the Study:

  • To investigate the relationship between CD80 costimulatory molecule expression and genomic methylation in non-inflammatory colon carcinogenesis.
  • To determine if altered methylation patterns correlate with reduced CD80 expression in colon tissues.
  • To assess the effect of DNA methyltransferase inhibition on CD80 expression in colon cancer cell lines.

Main Methods:

  • Quantification of DNA methyltransferases and CD80 mRNA expression using real-time qRT-PCR in colonic mucosal samples from healthy subjects and patients with dysplastic adenoma and colon adenocarcinoma.
  • Assessment of methylation status for key genes (CDH13, APC, MLH1, MGMT1, RUNX3) using methylation-specific PCR.
  • Evaluation of CD80 expression in colon cancer cell lines (HT29, HCT-15, LoVo) following treatment with the DNA-methyltransferase inhibitor 5-Aza-2'-deoxycytidine.

Main Results:

  • CD80 mRNA levels were significantly lower in non-inflammatory dysplastic colonic mucosa, particularly in patients with methylated genes.
  • A significant inverse correlation was observed between CD80 mRNA levels and patients' methylation scores.
  • Treatment with 5-Aza-2'-deoxycytidine significantly increased both CD80 mRNA levels and the proportion of CD80+ cells in colon cancer cell lines.

Conclusions:

  • Genomic methylation plays a role in the reduced expression of the costimulatory molecule CD80 during non-inflammatory colon carcinogenesis.
  • The findings suggest that methylation-mediated silencing of CD80 may contribute to the failure of immune surveillance in colon cancer.
  • Targeting DNA methylation could potentially restore CD80 expression and enhance anti-tumor immune responses.

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