HuR-regulated lncRNA NEAT1 stability in tumorigenesis and progression of ovarian cancer

被引:165
作者
Chai, Yiqing [1 ]
Liu, Jie [1 ]
Zhang, Zhikun [1 ]
Liu, Liwei [2 ]
机构
[1] Tianjin Cent Hosp Gynecol Obstet, Ultrasound Ctr, Tianjin 300052, Peoples R China
[2] Tianjin Med Univ, Hosp 2, Dept Urol, Tianjin 300211, Peoples R China
来源
CANCER MEDICINE | 2016年 / 5卷 / 07期
关键词
HuR; lncRNA; miR-124; NEAT1; ovarian cancer; LONG NONCODING RNA; POOR-PROGNOSIS; CELL-PROLIFERATION; HOTAIR PROMOTES; EXPRESSION; MICRORNA-124; CARCINOMA; MALAT1; MEG3; BIOMARKER;
D O I
10.1002/cam4.710
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Long noncoding RNAs (lncRNAs) have recently emerged as pivotal regulators in governing fundamental biological processes, as well as in tumorigenesis. The nuclear paraspeckle assembly transcript 1 (NEAT1) is one of the most highly regulated lncRNAs in recent genomic datasets, however, its biological role and regulatory mechanism in ovarian cancer (OC) development and progression are poorly defined. In this study, we identified that NEAT1 was up-regulated in OC patients and cell lines, and its expression was associated with the FIGO stage and lymph node metastasis. Furthermore, the ectopic expression of NEAT1_1 in OVCAR-3 cell lines promoted cell proliferation and invasion, whereas knockdown of NEAT1_1 did the opposite. Furthermore, NEAT1_1 was stabilized by an RNA-binding protein HuR, but suppressed by miR-124-3p in OC cells. Accordingly, the increased HuR mRNA and decreased miR-124-3p levels were observed in OC patients. These results suggested that lncRNA NEAT1, whose expression was collaboratively controlled by HuR and miR-124-3p, could regulate ovarian carcinogenesis and may serve as a potential target for antineoplastic therapies.
引用
收藏
页码:1588 / 1598
页数:11
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