MicroRNA-338 inhibits migration and proliferation by targeting hypoxia-induced factor 1α in nasopharyngeal carcinoma

被引:56
作者
Shan, Ying [1 ]
Li, Xingyu [2 ]
You, Bo [1 ]
Shi, Si [1 ]
Zhang, Qicheng [1 ]
You, Yiwen [1 ]
机构
[1] Nantong Univ, Affiliated Hosp, Dept Ear Nose & Throat, Nantong 226001, Jiangsu, Peoples R China
[2] Nantong Univ, Sch Med, Dept Pathol, Nantong 226001, Jiangsu, Peoples R China
基金
中国博士后科学基金;
关键词
miR-338-3p; metastasis; nasopharyngeal cancer; HIF-1; alpha; proliferation; EPITHELIAL-MESENCHYMAL TRANSITION; CANCER CELLS; INDUCIBLE FACTOR-1-ALPHA; HEPATOCELLULAR-CARCINOMA; SUPPRESSES INVASION; IN-VITRO; GROWTH; EXPRESSION; HIF-1-ALPHA; RADIOTHERAPY;
D O I
10.3892/or.2015.4195
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Nasopharyngeal cancer (NPC) is an endemic type of head and neck cancer with a high rate of cervical lymph node metastasis. An increasing number of studies have shown that microRNAs (miRNAs) play a key role in the development and progression of NPC. miR-338-3p has been demonstrated as an anti-oncogene in different solid tumors. The aim of the present study was to investigate the potential role of.miR-338-3p in the development and progression of NPC. Compared with normal samples, our data showed that miR-338-3p were downregulated in NPC tissues and cells. The luciferase assay demonstrated that HIF-1 alpha was a direct target of miR-338-3p. We also found that miR-338-3p regulated the expression levels of HIF-1 alpha, respectively. Overexpression of miR-338-3p in NPC cells significantly inhibited cell proliferation, and migration. Conversely, miR-338-3p knockdown in cells with lower endogenous expression levels significantly reduced antitumor behavior. Furthermore, enforced expression of miR-338-3p led to a decline in ERK phosphorylation as well as inhibited the hypoxia induced epithelial to mesenchymal transition. Cells pre-transfected with miR-338-3p can overcome hypoxiamediated cisplatin resistance. Taken together, we found that miR-338-3p directly targeted HIF-1 alpha, and we provide insight into NPC initiation and progression, possibly representing a novel therapeutic target.
引用
收藏
页码:1943 / 1952
页数:10
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