Circular RNA circNASP modulates the malignant behaviors in osteosarcoma via miR-1253/FOXF1 pathway

被引:64
作者
Huang, Lipeng [1 ]
Chen, Mangmang [1 ]
Pan, Jun [2 ]
Yu, Weiyang [3 ]
机构
[1] Wenzhou Med Univ, DingLi Clin Inst, Wenzhou Cent Hosp, Dept Orthopaed Surg, Wenzhou 325000, Peoples R China
[2] Wenzhou Med Univ, Affiliated Hosp 2, Dept Orthopaed Surg, Wenzhou 325000, Peoples R China
[3] Wenzhou Med Univ, Lishui Cent Hosp, Affiliated Hosp 5, Dept Orthopaed Surg, 289 Kuocang Rd, Lishui 323000, Zhejiang, Peoples R China
关键词
circNASP; Osteosarcoma; Proliferation; Cell cycle; Invasion; CELL-PROLIFERATION; CANCER; EXPRESSION; EXTREMITY; CARCINOMA; INVASION; FOXF1; CARCINOGENESIS; TRANSCRIPTION; PROGRESSION;
D O I
10.1016/j.bbrc.2018.04.131
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
Increasing evidences demonstrate that circular RNAs (circRNAs) serve as essential regulators in various human diseases, including cancer. However, the study on circRNA function in osteosarcoma (OS) is just emerging. In the present study, we screened out a novel circRNA termed circNASP which was significantly upregulated in OS tissues compared to adjacent normal tissues. We found that circNASP knockdown dramatically inhibited the proliferation, cell cycle progression and invasion of OS cells. Moreover, we showed that circNASP expression was positively correlated with tumor size and metastasis in OS patients. In terms of mechanism, we found that circNASP acts as a sponge of miR-1253 targeting FOXF1 in OS cells. By inhibiting miR-1253 availability, circNASP promoted FOXF1 expression. Rescue assays indicated that inhibition of miR-1253 could significantly reverse the effects of circNASP knockdown on OS cell proliferation and invasion while restoration of FOXF1 rescued the proliferation and invasion of OS cells transfected with miR-1253 mimics. Taken together, our findings demonstrated that circNASP contributes to malignant behaviors of OS cells by miR-1253/FOXF1 pathway, which suggested circNASP/miR-1253/FOXF1 axis might be a potential therapeutic target. (C) 2018 Elsevier Inc. All rights reserved.
引用
收藏
页码:511 / 517
页数:7
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