Promoter hypermethylation of Ras-related GTPase gene RRAD inactivates a tumor suppressor function in nasopharyngeal carcinoma

被引：43
|
作者：
Mo, Yingxi [1 ]
Midorikawa, Kaoru [1 ]
Zhang, Zhe [2 ]
Zhou, Xiaoying [2 ]
Ma, Ning [3 ]
Huang, Guangwu [2 ]
Hiraku, Yusuke [1 ]
Oikawa, Shinji [1 ]
Murata, Mariko [1 ]
机构：
[1] Mie Univ, Grad Sch Med, Dept Environm & Mol Med, Tsu, Mie, Japan
[2] Guangxi Med Univ, Affiliated Hosp 1, Dept Otolaryngol Head & Neck Surg, Nanning, Peoples R China
[3] Suzuka Univ Med Sci, Fac Hlth Sci, Matsusaka, Mie, Japan
来源：
CANCER LETTERS | 2012年 / 323卷 / 02期
关键词：
RRAD; Nasopharyngeal carcinoma; Methylation; ABERRANT METHYLATION; PATHOGENESIS; PROTEIN; MUSCLE; OVEREXPRESSION; GROWTH; CANCER; MEMBER; CELLS;
D O I：
10.1016/j.canlet.2012.03.042
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Nasopharyngeal carcinoma (NPC) is endemic in southern China. In a genome-wide screen for genes inactivated by promoter hypermethylation, we identified Ras-related associated with diabetes (RRAD). Expression of RRAD was down-regulated in 83.3% (30/36) of the biopsies from NPC patients. RRAD was aberrantly methylated in 74.3% (26/35) of primary tumors, but not in normal nasopharyngeal epithelium. Ectopic RRAD expression in NPC cell lines inhibited the cell growth, colony formation, and cell migration. These results indicate that RRAD might act as a functional tumor suppressor and its epigenetic inactivation may play an important role in NPC development. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：147 / 154
页数：8
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