Let-7a inhibits proliferation and induces apoptosis by targeting EZH2 in nasopharyngeal carcinoma cells

被引:38
作者
Cai, Kemin [1 ]
Wan, Yi [2 ]
Sun, Guan [3 ]
Shi, Lei [4 ]
Bao, Xueli [1 ]
Wang, Zhimin [2 ]
机构
[1] Taizhou Peoples Hosp, Dept Otorhinolaryngol Head & Neck Surg, Taizhou 225300, Jiangsu, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Suzhou Kowloon Hosp, Dept Neurosurg, Suzhou 215021, Peoples R China
[3] Nantong Univ, Affiliated Yancheng Hosp 4, Dept Neurosurg, Yancheng 224000, Peoples R China
[4] Jiangsu Univ, Peoples Hosp Kunshan 1, Dept Neurosurg, Suzhou 215300, Peoples R China
关键词
let-7a; enhancer of zeste homolog 2; proliferation; apoptosis; nasopharyngeal carcinoma; TUMOR-SUPPRESSOR; EXPRESSION; COMPLEX; CANCER; AGGRESSIVENESS; TUMORIGENESIS; ONTOLOGY; MIR-26A; PROTEIN; ROLES;
D O I
10.3892/or.2012.2027
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Let-7a is frequently downregulated in various types of human cancer including nasopharyngeal carcinoma. However, the underlying mechanism of let-7a action in nasopharyngeal carcinoma remains elusive. In this study, we show that the enhancer of zeste homolog 2 (EZH2) is a direct target of let-7a in human nasopharyngeal carcinoma cells. The inhibition of EZH2 in vitro by let-7a, EZH2 si RNA, attenuated nasopharyngeal carcinoma cell growth, inhibited cell proliferation and induced cell apoptosis. In addition, for each biological process we identified ontology-associated transcripts that significantly correlate with EZH2 expression. Finally, the expression of EZH2 significantly abrogated let-7a-mediated cell proliferation and apoptosis in the nasopharyngeal carcinoma cells. Taken together, our results suggest that let-7a and EZH2 may be potential therapeutic targets for nasopharyngeal carcinoma.
引用
收藏
页码:2101 / 2106
页数:6
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