Quantitative hypermethylation of NMDAR2B in human gastric cancer

Jun Wei Liu, Sook Kim Myoung, Jatin Nagpal, Keishi Yamashita, Luana Poeta, Xiaofei Chang, Juna Lee, Hannah Lui Park, Carmen Jeronimo, William H. Westra, Masaki Mori, Chulso Moon, Barry Trink, David Sidransky

Research output: Contribution to journalArticle

Abstract

NMDA receptor Type 2B (NMDAR2B) is a candidate TSG first identified in esophageal squamous cell carcinoma (ESCC). To evaluate NMDAR2B methylation in gastric cancer progression, we performed quantitative methylation-specitic PCR (MSP), RT-PCR and immnunohistochemistry (IHC) in primary gastric tissues and colony formation assays in gastric cancer cell lines. We found that the expression of NMDAR2B was reactivated by the demethylating agent, 5-aza-2′-deoxycytidine, with or without trichostatin A in gastric cancer cell lines. Moreover, inactivation of NMDAR2B was found to be closely correlated with promoter methylation status in gastric cell lines and primary gastric tumors. IHC data also showed that NMDAR2B was specifically expressed in gastric epithelial cells and its expression was diminished or absent in gastric cancer epithelium. Quantitative analysis of NMDAR2B promoter methylation showed 61% (17/28) hypermethylation in primary gastric tumors versus 5% (1/20) in normal gastric tissues from nongastric cancer patients. Forced overexpression of NMDAR2B in gastric cancer cell lines significantly inhibited cell colony formation. Taken together, the above results suggest that NMDAR2B methylation is a common and important biologically relevant event in gastric cancer progression.

Original languageEnglish (US)
Pages (from-to)1994-2000
Number of pages7
JournalInternational Journal of Cancer
Volume121
Issue number9
DOIs
StatePublished - Nov 1 2007

Keywords

  • Cancer
  • Gastric
  • Methylation
  • NMDAR2B

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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