| Literature DB >> 17620329 |
Jun-Wei Liu1, Myoung Sook Kim1, Jatin Nagpal1, Keishi Yamashita1, Luana Poeta1, Xiaofei Chang1, Juna Lee1, Hannah Lui Park1, Carmen Jeronimo1, William H Westra2, Masaki Mori3, Chulso Moon1, Barry Trink1, David Sidransky1.
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-specific 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 over-expression 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. Copyright (c) 2007 Wiley-Liss, Inc.Entities:
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Year: 2007 PMID： 17620329 DOI： 10.1002/ijc.22934
Source DB: PubMed Journal: Int J Cancer ISSN： 0020-7136 Impact factor: 7.396