Long noncoding RNA DLEU1 aggravates osteosarcoma carcinogenesis via regulating the miR-671-5p/DDX5 axis

被引:37
作者
Chen, Xinxin [1 ]
Zhang, Chengyong [2 ]
Wang, Xiao [1 ]
机构
[1] Henan Univ, Huaihe Hosp, Dept Orthoped, 8 Baobei Rd, Kaifeng 475000, Henan, Peoples R China
[2] Second Peoples Hosp Nanyang City, Dept Orthoped, Nanyang, Henan, Peoples R China
关键词
Osteosarcoma; DLEU1; miR-671-5p; DEAD-box helicase 5 (DDX5); oncogene; CELL-PROLIFERATION; PROMOTES PROLIFERATION; DDX5; CANCER; EXPRESSION; TUMORIGENESIS; CONTRIBUTES; MECHANISMS; INVASION;
D O I
10.1080/21691401.2019.1648285
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Long non-coding RNAs (LncRNAs) have been proven to be involved in the progression of osteosarcoma. LncRNA DLEU1 was found to act as an oncogene in various types of cancer. In this study, we aimed to explore the biological functions of DLEU1 in osteosarcoma and the specific mechanism. Our results showed that DLEU1 was highly expressed in osteosarcoma tissue specimens and cells. Downregulation of DLEU1 in osteosarcoma cells inhibited the cell proliferation, migration and invasion. Further mechanistic analysis and functional assays demonstrated that DLEU1 exerted its role by sponging microRNA (miR)-671-5p in osteosarcoma cells. Moreover, DEAD-box helicase 5 (DDX5) was confirmed as the target of miR-671-5p. Furthermore, rescue assays indicated that miR-671-5p inhibitor significantly reversed the effects of DLEU1 knockdown on osteosarcoma cell proliferation and invasion while restoration of DDX5 rescued the proliferation and invasion of osteosarcoma cells transfected with miR-671-5p mimics. In conclusion, DLEU1 acted as an oncogene in osteosarcoma by directly sponging miR-671-5p and regulating the expression of DDX5. These findings suggested that DLEU1 might be a novel therapeutic target in the treatment of osteosarcoma.
引用
收藏
页码:3322 / 3328
页数:7
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