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Updated: May 22, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
07:50

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

Published on: September 18, 2020

Epigenetic alteration of CCDC67 and its tumor suppressor function in gastric cancer

Sung-Joon Park1, Hay-Ran Jang, Mirang Kim

  • 1Medical Genomics Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Korea.

Carcinogenesis
|May 22, 2012
PubMed

Insights

Gastric cancer cells frequently show silenced coiled-coil domain-containing 67 (CCDC67) due to promoter methylation. Restoring CCDC67 expression suppressed tumor growth, suggesting it is a tumor suppressor gene.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Gastric cancer is a significant global health concern.
  • Epigenetic alterations, particularly promoter methylation, play a crucial role in cancer development.
  • The function of coiled-coil domain-containing 67 (CCDC67) in gastric tumorigenesis is largely unknown.

Purpose of the Study:

  • To investigate the role of CCDC67 in gastric cancer.
  • To determine if CCDC67 promoter methylation is associated with its gene expression in gastric cancer.
  • To evaluate the functional impact of CCDC67 on gastric cancer cell behavior and tumorigenesis.

Main Methods:

  • Restriction landmark genomic scanning and pyrosequencing were used to analyze CCDC67 promoter methylation.
  • Gene expression levels were assessed in gastric cancer cell lines and primary tumors.
  • Functional assays included cell adhesion, colony formation, and in vivo tumorigenesis studies in nude mice.
  • Treatment with epigenetic modifiers (5-aza-2'-deoxycytidine and trichostatin A) was employed to assess CCDC67 re-expression.

Main Results:

  • CCDC67 promoter CpG hypermethylation was frequently observed in gastric cancer cell lines (72.7%) and primary tumors (74%).
  • CCDC67 gene expression was significantly down-regulated in most gastric cancer samples, correlating with promoter hypermethylation.
  • Restoration of CCDC67 expression via epigenetic drug treatment reactivated the gene.
  • Overexpression of CCDC67 inhibited colony formation and suppressed tumor growth in vivo, indicating a tumor-suppressive role.

Conclusions:

  • CCDC67 is identified as a putative tumor suppressor gene in gastric cancer.
  • Silencing of CCDC67 by promoter CpG methylation is a key mechanism in gastric tumorigenesis.
  • CCDC67 may be involved in cell signaling and migration pathways critical for tumor development.

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