Microarray profiles reveal that circular RNA hsa_circ_0007385 functions as an oncogene in non-small cell lung cancer tumorigenesis

被引:108
作者
Jiang, Ming-Ming [1 ]
Mai, Zhi-Tao [1 ]
Wan, Shan-Zhi [1 ]
Chi, Yu-Min [1 ]
Zhang, Xin [1 ]
Sun, Bao-Hua [1 ]
Di, Qing-Guo [1 ]
机构
[1] Cangzhou Cent Hosp, Dept Respirat, Xinhua Rd 201, Cangzhou City 061001, Hebei, Peoples R China
关键词
Non-small cell lung cancer; Circular RNA; Hsa_circ_0007385; Oncogene; MiR-181; NONCODING RNA; EXPRESSION; PROLIFERATION; BIOMARKERS; MEMBER;
D O I
10.1007/s00432-017-2576-2
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Circular RNAs (circRNAs) are a novel class of non-protein-coding RNA. Emerging evidence indicates that circRNAs participate in the regulation of many pathophysiological processes. This study aims to explore the expression profiles and pathological effects of circRNAs in non-small cell lung cancer (NSCLC). Human circRNAs microarray analysis was performed to screen the expression profile of circRNAs in NSCLC tissue. Expressions of circRNA and miRNA in NSCLC tissues and cells were quantified by qRTPCR. Functional experiments were performed to investigate the biological functions of circRNA, including CCK-8 assay, colony formation assay, transwell assay and xenograft in vivo assay. Human circRNAs microarray revealed a total 957 abnormally expressed circRNAs (> twofold, P < 0.05) in NSCLC tissue compared with adjacent normal tissue. In further studies, hsa_circ_0007385 was significantly up regulated in NSCLC tissue and cells. In vitro experiments with hsa_circ_0007385 knockdown resulted in significant suppression of the proliferation, migration and invasion of NSCLC cells. In vivo xenograft assay using hsa_circ_0007385 knockdown, significantly reduced tumor growth. Bioinformatics analysis and luciferase reporter assay verified the potential target miR-181, suggesting a possible regulatory pathway for hsa_circ_0007385. In summary, results suggest hsa_circ_0007385 plays a role in NSCLC tumorigenesis, providing a potential therapeutic target for NSCLC.
引用
收藏
页码:667 / 674
页数:8
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