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

研究成果: ジャーナルへの寄稿記事

38 引用 (Scopus)

抄録

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.

元の言語英語
ページ(範囲)1994-2000
ページ数7
ジャーナルInternational Journal of Cancer
121
発行部数9
DOI
出版物ステータス出版済み - 11 1 2007

Fingerprint

Stomach Neoplasms
Stomach
Methylation
Cell Line
decitabine
trichostatin A
Neoplasms
Polymerase Chain Reaction
NR2B NMDA receptor
Epithelium
Epithelial Cells

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

これを引用

Liu, J. W., Myoung, S. K., Nagpal, J., Yamashita, K., Poeta, L., Chang, X., ... Sidransky, D. (2007). Quantitative hypermethylation of NMDAR2B in human gastric cancer. International Journal of Cancer, 121(9), 1994-2000. https://doi.org/10.1002/ijc.22934

Quantitative hypermethylation of NMDAR2B in human gastric cancer. / Liu, Jun Wei; Myoung, Sook Kim; Nagpal, Jatin; Yamashita, Keishi; Poeta, Luana; Chang, Xiaofei; Lee, Juna; Park, Hannah Lui; Jeronimo, Carmen; Westra, William H.; Mori, Masaki; Moon, Chulso; Trink, Barry; Sidransky, David.

:: International Journal of Cancer, 巻 121, 番号 9, 01.11.2007, p. 1994-2000.

研究成果: ジャーナルへの寄稿記事

Liu, JW, Myoung, SK, Nagpal, J, Yamashita, K, Poeta, L, Chang, X, Lee, J, Park, HL, Jeronimo, C, Westra, WH, Mori, M, Moon, C, Trink, B & Sidransky, D 2007, 'Quantitative hypermethylation of NMDAR2B in human gastric cancer', International Journal of Cancer, 巻. 121, 番号 9, pp. 1994-2000. https://doi.org/10.1002/ijc.22934
Liu JW, Myoung SK, Nagpal J, Yamashita K, Poeta L, Chang X その他. Quantitative hypermethylation of NMDAR2B in human gastric cancer. International Journal of Cancer. 2007 11 1;121(9):1994-2000. https://doi.org/10.1002/ijc.22934
Liu, Jun Wei ; Myoung, Sook Kim ; Nagpal, Jatin ; Yamashita, Keishi ; Poeta, Luana ; Chang, Xiaofei ; Lee, Juna ; Park, Hannah Lui ; Jeronimo, Carmen ; Westra, William H. ; Mori, Masaki ; Moon, Chulso ; Trink, Barry ; Sidransky, David. / Quantitative hypermethylation of NMDAR2B in human gastric cancer. :: International Journal of Cancer. 2007 ; 巻 121, 番号 9. pp. 1994-2000.
@article{d28aaa994a884fb1964a8580514af9e7,
title = "Quantitative hypermethylation of NMDAR2B in human gastric cancer",
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.",
author = "Liu, {Jun Wei} and Myoung, {Sook Kim} and Jatin Nagpal and Keishi Yamashita and Luana Poeta and Xiaofei Chang and Juna Lee and Park, {Hannah Lui} and Carmen Jeronimo and Westra, {William H.} and Masaki Mori and Chulso Moon and Barry Trink and David Sidransky",
year = "2007",
month = "11",
day = "1",
doi = "10.1002/ijc.22934",
language = "English",
volume = "121",
pages = "1994--2000",
journal = "International Journal of Cancer",
issn = "0020-7136",
publisher = "Wiley-Liss Inc.",
number = "9",

}

TY - JOUR

T1 - Quantitative hypermethylation of NMDAR2B in human gastric cancer

AU - Liu, Jun Wei

AU - Myoung, Sook Kim

AU - Nagpal, Jatin

AU - Yamashita, Keishi

AU - Poeta, Luana

AU - Chang, Xiaofei

AU - Lee, Juna

AU - Park, Hannah Lui

AU - Jeronimo, Carmen

AU - Westra, William H.

AU - Mori, Masaki

AU - Moon, Chulso

AU - Trink, Barry

AU - Sidransky, David

PY - 2007/11/1

Y1 - 2007/11/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=34648833479&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34648833479&partnerID=8YFLogxK

U2 - 10.1002/ijc.22934

DO - 10.1002/ijc.22934

M3 - Article

C2 - 17620329

AN - SCOPUS:34648833479

VL - 121

SP - 1994

EP - 2000

JO - International Journal of Cancer

JF - International Journal of Cancer

SN - 0020-7136

IS - 9

ER -