[Mechanism of loss of human esophageal cancer-related gene 4 (ECRG4) gene expression in esophageal squamous cell carcinoma cell line EC9706]

Zhonghua Zhong Liu Za Zhi. 2011 Aug;33(8):570-3.
[Article in Chinese]

Abstract

Objective: To investigate the mechanism of loss of human esophageal cancer-related gene 4 (ECRG4) expression in esophageal squamous cell carcinoma (ESCC.)

Methods: PCR-SSCP and DNA sequencing analysis were used to detect the mutation of ECRG4 exons in esophageal cancer and matched adjacent normal tissues of 80 patients. DNA bisulfite-modifying ssPCR sequencing assay was used to examine the methylation status of ECRG4 promoter in human esophageal squamous cell carcinoma EC9706 cells. The re-expression of ECRG4 mRNA was examined by RT-PCR in EC9706 cells, after treatment with either demethylation drug 5-aza-2'-deoxycytidine or arsenic trioxide.

Results: No mutation in the four ECRG4 exons was found in all the ESCC and matched normal adjacent tissues. RT-PCR showed that 11 of 16 CpG islands of ECRG4 promoter were hypermethylated, while ECRG4 mRNA expression level was undetectable in the EC9706 cells. The ECRG4 mRNA was re-expressed after treatment with either demethylation drug 5-aza-2'-deoxycytidine or arsenic trioxide.

Conclusion: The epigenetic mechanism of methylation is a reason of loss of ECRG4 gene expression in the ESCC cell line EC9706.

MeSH terms

  • Antimetabolites, Antineoplastic / pharmacology
  • Antineoplastic Agents / pharmacology
  • Arsenic Trioxide
  • Arsenicals / pharmacology
  • Azacitidine / analogs & derivatives
  • Azacitidine / pharmacology
  • Carcinoma, Squamous Cell / genetics
  • Carcinoma, Squamous Cell / metabolism*
  • Carcinoma, Squamous Cell / pathology
  • Cell Line, Tumor
  • CpG Islands / genetics*
  • DNA Methylation*
  • Decitabine
  • Epigenesis, Genetic
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / metabolism*
  • Esophageal Neoplasms / pathology
  • Exons
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Mutation
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • Oxides / pharmacology
  • Promoter Regions, Genetic
  • RNA, Messenger / metabolism
  • Tumor Suppressor Proteins

Substances

  • Antimetabolites, Antineoplastic
  • Antineoplastic Agents
  • Arsenicals
  • ECRG4 protein, human
  • Neoplasm Proteins
  • Oxides
  • RNA, Messenger
  • Tumor Suppressor Proteins
  • Decitabine
  • Azacitidine
  • Arsenic Trioxide