Effect of miR-135b inhibitor on biological characteristics of osteosarcoma cells through up-regulating PPM1A

被引:2
|
作者
Gao, Junsheng [1 ,2 ]
Zhang, Lu [2 ]
Liu, Zhiang [2 ]
Yao, Shuaihui [2 ]
Gao, Songming [2 ]
Wang, Limin [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Orthoped, Zhengzhou, Henan, Peoples R China
[2] Peoples Hosp Zhengzhou, Dept Orthoped, Zhengzhou, Henan, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY | 2019年 / 12卷 / 03期
关键词
miR-135b; protein phosphatase Mg2+/Mn2+ dependent 1A; osteosarcoma; proliferation; invasion; PROMOTES PROLIFERATION; INVASION; METASTASIS; MIGRATION; EXPRESSION; CATENIN;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
miR-135b is expressed abnormally in various tumors and plays an important role in the occurrence and development of tumors bydifferent pathways. The role of miR-135b in osteosarcoma (OS) and its mechanisms were uncertain. The study aimed to clarify the role of miR-135b in osteosarcoma (OS) cells and explore the effect of miR-135b inhibitor on the biological characteristics of OS cells. Firstly, Compared with adjacent bone tissues, the expression of miR-135b was increased and inversely correlated with potential target-PPM1A mRNA, while the expression of PPM1A was decreased in OS tissues. Dual luciferase reporter assay was used to verify that PPM1A was a target gene of miR-135b and RT-PCR and western blot were used to detect that miR-135b negatively regulated expression of PPM1A in MG63 and U2OS cell lines. After transfection, miR-135b inhibitor significantly inhibited cell proliferation and invasion both in MG63 and U2OS cells and blocked cell cycle in the G2/M phase and induced cells apoptosis, while PPM1A knockdown abolished the inhibition of miR-135b inhibitor on the proliferation and invasion of OS cells. In conclusion, miR-135b is up-regulated in OS cells and down regulating miR-135b expression could inhibit the proliferation and invasion of OS cells by up-regulating PPM1A. miR-135b might be a new therapeutic target of OS.
引用
收藏
页码:689 / 699
页数:11
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