MicroRNA-101 inhibits proliferation, migration and invasion in osteosarcoma cells by targeting ROCK1

被引:3
|
作者
Jiang, Rui [1 ]
Zhang, Chao [2 ]
Liu, Guangyao [1 ]
Gu, Rui [1 ]
Wu, Han [1 ]
机构
[1] Jilin Univ, Dept Orthoped, China Japan Union Hosp, 126 Xiantai St, Changchun 130033, Jilin Province, Peoples R China
[2] Jilin Univ, Dept Ophthalmol, Hosp 2, Changchun 130041, Peoples R China
来源
AMERICAN JOURNAL OF CANCER RESEARCH | 2017年 / 7卷 / 01期
关键词
Osteosarcoma; microRNA-101; ROCK1; cell apoptosis; cell migration; POTENTIAL THERAPEUTIC TARGET; DOWN-REGULATION; GASTRIC-CANCER; TUMOR-GROWTH; SUPPRESSES; METASTASIS; EXPRESSION; CARCINOMA; MIR-101;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Osteosarcoma is a rare malignant bone tumor in adolescents, with high degree of malignancy, and highly incidence of recurrence and metastasis. Our study aimed to explore the role of miR-101 in osteosarcoma cells by targeting ROCK1. In the present study, reverse transcription-quantitative polymerase chain reaction data revealed that miR-101 was down-regulated in the tissue samples of 20 patients with osteosarcoma compared with their matched adjacent non-tumor tissues (P < 0.01). Furthermore, miR-101 was significantly down-regulated in three common OS cell lines, MG63, U2OS, and OS732 compared with the human osteoblast cell line, hFOB1.19 (P < 0.01). MiR-101 was shown to target the ROCK1 3'-UTR in dual-luciferase reporter assays in MG63 cells. Overexpression of miR-101 significantly suppressed the protein expression levels of ROCK1, while knockdown of miR-101 significantly enhanced the formers' expression levels in MG63 cells (P < 0.05). Overexpression of miR-101 inhibited cell viability, migration, and invasion while promoted apoptosis. Independent inhibition of ROCK1 and knockdown of miR-101 expression levels significantly promoted MG63 cell proliferation, migration and invasion while inhibited apoptosis (P < 0.01). Moreover, knockdown of ROCK1 reversed the promotion effect of miR-101 knockdown on proliferation, migration, and invasion while promoted apoptosis of MG63 cells, suggesting that miR-101 acts as a tumor suppressor in osteosarcoma cells via targeting ROCK1. Furthermore, overexpression of miR-101 inhibited tumor growth and motion by inactivating PI3K/AKT and JAK/STAT signaling pathways via downregulation of ROCK1. To conclude, miR-101/ROCK1 may be a potential therapeutic target for osteosarcoma therapy.
引用
收藏
页码:88 / 97
页数:10
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