A novel circular RNA, hsa-circ-0000211, promotes lung adenocarcinoma migration and invasion through sponging of hsa-miR-622 and modulating HIF1-α expression

被引:29
作者
Feng, Dongjie
Xu, Youtao
Hu, Jingwen
Zhang, Shuai
Li, Ming
Xu, Lin
机构
[1] Nanjing Med Univ, Jiangsu Canc Hosp, Dept Thorac Surg, Nanjing 210009, Peoples R China
[2] Nanjing Med Univ, Jiangsu Inst Canc Res, Nanjing 210009, Peoples R China
[3] Nanjing Med Univ, Affiliated Canc Hosp, Nanjing 210009, Peoples R China
基金
中国国家自然科学基金;
关键词
Circular RNA; hsa-circ-0000211; Lung adenocarcinoma; miR-622; sponge; hypoxia-inducible factor 1 alpha; HYPOXIA; PROLIFERATION; CELLS;
D O I
10.1016/j.bbrc.2019.10.134
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
Recently, several studies have evaluated the role of circular RNAs in the metastasis and development of multiple cancers. In our earlier microarray-based study, we had reported the aberrant expression of a novel circular RNA, hsa-circ-0000211 in lung adenocarcinoma (LAC) tissues. However, the roles of hsa-circ-0000211 in LAC have not been studied. Here hsa-circ-0000211 expression in the LAC tissues and cell lines was determined by quantitative real-time PCR (qRT-PCR). The function of hsa-circ-0000211 was evaluated by transwell assay and wound healing. Mechanisms of hsa-circ-0000211 was measured by luciferase reporter assay and western blot. Results revealed the expression of hsa-circ-0000211 in the human LAC tissues and LAC cell lines was higher than that in normal tissue and human lung normal epithelial cells, respectively. The knockdown of hsa-circ-0000211 could inhibit the migration and invasion properties of LAC. Furthermore, hsa-circ-0000211 promoted the migration and invasion of LAC by sponging miR-622. Moreover, hsa-circ-0000211 upregulated the HIF1-alpha expression by targeting miR-622. hsa-circ-0000211 promoted LAC cell migration and invasion by modulating the miR-622/HIF1-alpha network. Our study demonstrated that hsa-circ-0000211 can be a potential novel therapeutic target for LAC. (C) 2019 Published by Elsevier Inc.
引用
收藏
页码:395 / 401
页数:7
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