DNA copy number gain-mediated lncRNA LINC01061 upregulation predicts poor prognosis and promotes papillary thyroid cancer progression

被引:16
|
作者
Wu, Xinhua [1 ]
Yan, Yan [1 ]
Li, Hang [1 ]
Ji, Ning [1 ]
Yu, Tao [1 ]
Huang, Yujie [1 ]
Shi, Wen [1 ]
Gao, Lingcheng [1 ]
Ma, Liming [1 ]
Hu, Yunshu [2 ]
机构
[1] Huaian Hosp Huaian Dist, Dept Endocrinol, Huaian 223200, Jiangsu, Peoples R China
[2] Xinan Hosp, Dept Lab, Huaian 223200, Jiangsu, Peoples R China
关键词
Copy number amplification; Papillary thyroid cancer; Long noncoding RNA; Progression; LINC01061; SIGNALING ACTIVATION; CARCINOMA; EXPRESSION; PROLIFERATION; INVASION; CELLS; CERNA;
D O I
10.1016/j.bbrc.2018.07.032
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Several DNA copy number amplifications (CNAs) have been reported in papillary thyroid cancer (PTC). However, the functional role of CNAs in PTC remains very unclear. And whether there is a correlation between long noncoding RNA (IncRNA) and CNA requires to be explored. Here, we identified a novel IncRNA LINC01061. The genomic copy number of LINC01061 is amplified, which leads to its elevated expression level in PTC tissues. Moreover, increased level of LINC01061 was correlated with aggressive clinicopathological characteristics. Functional study indicated that LINC01061 silence significantly inhibited the proliferation, cell-cycle and invasion of PTC cells in vitro and tumor growth in vivo. Mechanistically, we showed that LINC01061 interacted with miR-4316 to promote E2F6 expression. The expression of miR-4316 was downregulated in PTC tissues while that of E2F6 was upregulated. Through rescue assay, we demonstrated that LINC01061 promoted PTC cell proliferation, cell-cycle progression and invasion by regulating miR-4316/E2F6 signaling pathway. In conclusion, our research indicated that LINC01061 might be a target for PTC therapy. (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码:1247 / 1253
页数:7
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