[Aberrant methylation of T-cadherin gene in human esophageal carcinoma cells]

Zhonghua Yi Xue Za Zhi. 2011 Oct 11;91(37):2653-6.
[Article in Chinese]

Abstract

Objective: To explore the methylation status of T-cadherin promoter region in human esophageal carcinoma cell lines EC1 and EC109 and elucidate the effects of 5-azacytidine-2'-deoxycytidine (5-Aza-CdR) on their abilities of proliferation and invasion, the methylation status and the expression of T-cadherin.

Methods: The expression level of T-cadherin was measured by Western blot. And the methylation status of T-cadherin promoter region was analyzed by methylation-specific PCR (polymerase chain reaction), separately before and after a treatment of demethylating agent 5-Aza-CdR.

Results: The T-cadherin gene was hypermethylated in EC109 cells but semi-methylated in EC1 cells. After a treatment of 5-Aza-CdR, T-cadherin gene methylation was reversed. And the gene expression was strongly up-regulated in both cells. 5-Aza-CdR could decrease the proliferation and effectively inhibit the ability of cell invasion (P < 0.01).

Conclusion: The aberrant methylation in promoter region is an important mechanism of T-cadherin gene inactivation in human esophageal carcinoma cells. 5-Aza-CdR can increase the expression of T-cadherin by a reversal of hypermethylation and effectively inhibit the proliferation and invasion of tumor cells.

Publication types

  • English Abstract

MeSH terms

  • Azacitidine / pharmacology
  • Cadherins / genetics
  • Cadherins / metabolism*
  • Cell Line, Tumor
  • DNA Methylation*
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / metabolism*
  • Esophageal Neoplasms / pathology
  • Humans
  • Promoter Regions, Genetic*

Substances

  • Cadherins
  • Azacitidine