PMID- 21639937
OWN - NLM
STAT- MEDLINE
DCOM- 20111031
LR  - 20211020
IS  - 1471-2407 (Electronic)
IS  - 1471-2407 (Linking)
VI  - 11
DP  - 2011 Jun 5
TI  - Aberrant methylation of N-methyl-D-aspartate receptor type 2B (NMDAR2B) in 
      non-small cell carcinoma.
PG  - 220
LID - 10.1186/1471-2407-11-220 [doi]
AB  - BACKGROUND: N-methyl-D-aspartate receptors (NMDAR) act as tumor suppressors of 
      digestive malignancies. The expression and genetic methylation patterns of 
      NMDAR2B in non-small cell lung cancer (NSCLC) are unknown. METHODS: The 
      relationship between gene methylation and expression of NMDAR2B was analyzed in 
      NSCLC cell lines (N = 9) and clinical tissues (N = 216). The cell lines were 
      studied using RT-PCR and 5-aza-2'-deoxycytidine treatment, while the clinical 
      tissues were examined by methylation specific real-time quantitative PCR and 
      immunohistochemistry. Retrospective investigation of patient records was used to 
      determine the clinical significance of NMDAR2B methylation. RESULTS: NMDAR2B was 
      silenced in five of the nine cell lines; 5-aza-2'-deoxycytidine treatment 
      restored expression, and was inversely correlated with methylation. Aberrant 
      methylation of NMDAR2B, detected in 61% (131/216) of clinical NSCLC tissues, was 
      inversely correlated with the status of protein expression in 20 randomly 
      examined tumors. Aberrant methylation was not associated with clinical factors 
      such as gender, age, histological type, or TNM stage. However, aberrant 
      methylation was an independent prognostic factor in squamous cell carcinoma 
      cases. CONCLUSIONS: Aberrant methylation of the NMDAR2B gene is a common event in 
      NSCLC. The prognosis was significantly better for cases of squamous cell 
      carcinoma in which NMDAR2B was methylated. It may have different roles in 
      different histological types.
FAU - Tamura, Hajime
AU  - Tamura H
AD  - Department of General Thoracic Surgery, Graduate School of Medicine, Chiba 
      University, 1-8-1 Inohana, Chuoh-Ku, Chiba 280-8670, Japan.
FAU - Suzuki, Makoto
AU  - Suzuki M
FAU - Moriya, Yasumitsu
AU  - Moriya Y
FAU - Hoshino, Hidehisa
AU  - Hoshino H
FAU - Okamoto, Tatsuro
AU  - Okamoto T
FAU - Yoshida, Shigetoshi
AU  - Yoshida S
FAU - Yoshino, Ichiro
AU  - Yoshino I
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110605
PL  - England
TA  - BMC Cancer
JT  - BMC cancer
JID - 100967800
RN  - 0 (NR2B NMDA receptor)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Neoplasm)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 776B62CQ27 (Decitabine)
RN  - M801H13NRU (Azacitidine)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Azacitidine/analogs & derivatives/pharmacology
MH  - Carcinoma, Non-Small-Cell Lung/epidemiology/*genetics/metabolism/surgery
MH  - Carcinoma, Squamous Cell/epidemiology/genetics/metabolism/surgery
MH  - Cell Line, Tumor/drug effects/metabolism
MH  - *DNA Methylation/drug effects
MH  - Decitabine
MH  - Female
MH  - *Gene Expression Regulation, Neoplastic/drug effects
MH  - Humans
MH  - Japan/epidemiology
MH  - Lung Neoplasms/epidemiology/*genetics/metabolism/surgery
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Proteins/biosynthesis/*genetics
MH  - Neoplasm Staging
MH  - Pneumonectomy
MH  - Prognosis
MH  - Proportional Hazards Models
MH  - RNA, Messenger/biosynthesis
MH  - RNA, Neoplasm/biosynthesis
MH  - Receptors, N-Methyl-D-Aspartate/biosynthesis/*genetics
MH  - Sampling Studies
PMC - PMC3149028
EDAT- 2011/06/07 06:00
MHDA- 2011/11/01 06:00
PMCR- 2011/06/05
CRDT- 2011/06/07 06:00
PHST- 2010/09/16 00:00 [received]
PHST- 2011/06/05 00:00 [accepted]
PHST- 2011/06/07 06:00 [entrez]
PHST- 2011/06/07 06:00 [pubmed]
PHST- 2011/11/01 06:00 [medline]
PHST- 2011/06/05 00:00 [pmc-release]
AID - 1471-2407-11-220 [pii]
AID - 10.1186/1471-2407-11-220 [doi]
PST - epublish
SO  - BMC Cancer. 2011 Jun 5;11:220. doi: 10.1186/1471-2407-11-220.