MicroRNA-466 inhibits osteosarcoma cell proliferation and induces apoptosis by targeting CCND1

被引:17
|
作者
Cao, Wei [1 ]
Fang, Le [2 ]
Teng, Siyong [3 ]
Chen, Hongwei [4 ]
Liu, Tiejun [5 ]
机构
[1] Capital Med Univ, Beijing Rehabil Hosp, Clin Lab, Beijing 100041, Peoples R China
[2] 521 Hosp Ordnance Ind, Dept Blood Transfus, Xian 710065, Shaanxi, Peoples R China
[3] Natl Ctr Cardiovasc Dis, Dept Cardiovasc Med, Beijing 102300, Peoples R China
[4] Shanghai Songjiang Dist Cent Hosp, Clin Lab, Shanghai 201600, Peoples R China
[5] Capital Med Univ, Beijing Rehabil Hosp, Dept Urol, Badachu Rd, Beijing 100144, Peoples R China
关键词
miR-466; CCND1; proliferation; apoptosis; osteosarcoma; DOWN-REGULATION; EXPRESSION; CANCER; INVASION; GROWTH;
D O I
10.3892/etm.2018.6888
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Emerging pieces of evidence indicate that microRNA-466 (miR-466) serves as a tumor suppressor in several human tumors, including colorectal cancer and prostate cancer. However, whether miR-466 is involved in osteosarcoma (OS) progression remains largely unknown. The present study demonstrated that miR-466 was significantly downregulated in OS tissues and cell lines. Furthermore, it was revealed that the expression of miR-466 was negatively correlated with OS severity. Moreover, low miR-466 expression in patients with OS predicted poor prognosis. Through functional experiments, miR-466 overexpression significantly inhibited the proliferation and cell cycle of OS cells while inducing cellular apoptosis. In terms of mechanism, it was revealed that CCND1 was a target of miR-466 in OS cells. miR-466 overexpression suppressed CCND1 expression in OS cells. A reverse association was observed between the expression levels of miR-466 and CCND1 in OS tissues. Furthermore, CCND1 restoration in OS cells significantly rescued the effects of miR-466 on cellular proliferation and apoptosis. Overall, the results of the present study demonstrated that miR-466 suppressed OS progression by targeting CCND1, suggesting that miR-466 may be a promising biomarker and therapeutic target for OS prognosis and treatment.
引用
收藏
页码:5117 / 5122
页数:6
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