Long Noncoding RNA LINC0086 Functions as a Tumor Suppressor in Nasopharyngeal Carcinoma by Targeting miR-214

被引:41
作者
Guo, Jie [1 ,2 ]
Ma, Jinqi [3 ]
Zhao, Guosheng [3 ]
Li, Guocai [3 ]
Fu, Yunfeng [3 ]
Luo, Yanwei [3 ]
Gui, Rong [3 ]
机构
[1] Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol South China, Dept Prevent Oncol, Guangzhou, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Sch Publ Hlth, Dept Med Stat & Epidemiol, Guangzhou, Guangdong, Peoples R China
[3] Cent S Univ, Xiangya Hosp 3, Dept Blood Transfus, 138 Tongzipo Rd, Changsha 410013, Hunan, Peoples R China
关键词
Nasopharyngeal carcinoma (NPC); Long noncoding RNAs (lncRNAs); LINC0086; miR-214; Carcinogenesis; MESENCHYMAL TRANSITION; CANCER; METASTASIS; EXPRESSION; PROMOTES; RADIORESISTANCE; INVASION; ROLES; CELLS;
D O I
10.3727/096504017X14865126670075
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Nasopharyngeal carcinoma (NPC) is a distinct head and neck cancer, which is occurring at a high frequency in Southern China. Emerging studies have shown that long noncoding RNAs (lncRNAs) play a critical role in carcinogenesis and progression. In this study, we established a comprehensive lncRNA profile in NPC and found that 35 lncRNAs were differentially expressed in NPC. We found that LINC0086 was decreased in NPC patient serum samples and tissues. The Kaplan-Meier survival curve showed that patients with high LINC0086 expression had a higher survival rate than those with low LINC0086 expression. LINC0086 expression was associated with NPC histological grade, lymph node metastasis, and clinical stage. Upregulation of LINC0086 inhibited cancer cell proliferation and promoted apoptosis. In addition, upregulation of LINC0086 dramatically decreased the expression of miR-214, an oncogene in several cancers, in C666-1 and HK-1 cells. An miR-214 binding site was found in the 3'-UTR of LINC0086. We also validated that both miR-214 and LINC0086 presented in the RISC complex, demonstrating that LINC0086 could decrease miR-214 expression by directly interacting with miR-214. Furthermore, the suppressive effects of LINC0086 on NPC cell growth were reversed by overexpression of miR-214 in vitro and in vivo. Thus, our study reports a novel mechanism underlying NPC carcinogenesis and provides a potential novel diagnosis and treatment biomarker for NPC.
引用
收藏
页码:1189 / 1197
页数:9
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