5-Aza-2'-deoxycitydine induces demethylation and up-regulates transcription of p16INK4A gene in human gastric cancer cell lines

Chin Med J (Engl). 2004 Jan;117(1):99-103.

Abstract

Background: To investigate the effects of DNA methylation on the expression of tumor-associated genes and the cell cycle in human gastric cancer cells.

Methods: Two gastric cancer cell lines (MKN-45 and HGC-27) were treated with DNA methyltransferase (DNMT) inhibitor, 5-aza-2'-deoxycytidine (5-aza-dC). The expressions of p16INK4A, p21WAF1, p53, p73, c-Ha-ras and c-myc genes mRNA were detected by using reverse transcription PCR (RT-PCR). DNA methylation status of p16INK4A gene promoter was assayed by bisulfite modification and sequencing. The cell cycle was analyzed by using flow cytometry (FCM).

Results: 5-aza-dC induced the demethylation of p16INK4A gene promoter. The expression of p16INK4A mRNA was obviously up-regulated by treatment with 10 micro mol/L (MKN-45 cells) or 5 micro mol/L (HGC-27 cells) of 5-aza-dC for 24 hours. However, 5-aza-dC treatment failed to regulate the expressions of p21WAF1, p53, p73, c-Ha-ras and c-myc genes in MKN-45 and HGC-27 cells. Furthermore, 5-aza-dC induced the cell cycle arrest in G1 phase in HGC-27 cell, but not in MKN-45 cell.

Conclusions: DNA methylation regulates the transcription of p16INK4A but not p21WAF1 and proto-oncogenes in human gastric cancer cell lines MKN-45 and HGC-27.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Azacitidine / analogs & derivatives*
  • Azacitidine / pharmacology*
  • Cell Line, Tumor
  • DNA Methylation
  • Decitabine
  • Enzyme Inhibitors / pharmacology*
  • Flow Cytometry
  • Gene Expression
  • Genes, Tumor Suppressor / physiology
  • Genes, p16 / physiology*
  • Humans
  • Reverse Transcriptase Polymerase Chain Reaction
  • Stomach Neoplasms / genetics*
  • Transcription, Genetic*
  • Up-Regulation

Substances

  • Enzyme Inhibitors
  • Decitabine
  • Azacitidine