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miR-23a suppresses proliferation of osteosarcoma cells by targeting SATB1
被引:40
作者:
Wang, Guangbin
[1
]
Li, Bin
[1
]
Fu, Yonghui
[1
]
He, Ming
[1
]
Wang, Jiashi
[1
]
Shen, Peng
[1
]
Bai, Lunhao
[1
]
机构:
[1] China Med Univ, Shengjing Hosp, Dept Orthoped, Shenyang 110004, Liaoning, Peoples R China
基金:
美国国家科学基金会;
关键词:
miR-23a;
Osteosarcoma;
Proliferation;
SATB1;
UP-REGULATION;
TUMOR-GROWTH;
PROMOTES;
CANCER;
MICRORNA-23A;
METASTASIS;
EXPRESSION;
GENE;
REGULATOR;
INVASION;
D O I:
10.1007/s13277-015-3120-0
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Accumulating evidence has shown that microRNAs are involved in multiple processes in cancer development and progression. Recent studies have shown that miR-23a functions as an oncogene in various human cancer types, but its role in osteosarcoma remains poorly understood. Here, we demonstrated that miR-23a is frequently downregulated in osteosarcoma specimens and cell lines compared with adjacent noncancerous tissues and cell line. Bioinformatics analysis further revealed SATB1 as a potential target of miR-23a. Data from luciferase reporter assays showed that miR-23a directly binds to the 3'UTR of SATB1 messenger RNA (mRNA). Furthermore, we found that expression patterns of miR-23a were inversely correlated with those of SATB1 in osteosarcoma tissues and cell lines, and overexpression of miR-23a suppressed SATB1 expression at both transcriptional and translational levels in osteosarcoma cell lines. In functional assays, miR-23a inhibited osteosarcoma cell proliferation, which could be reversed by overexpression of SATB1. Furthermore, knockdown of SATB1 reduced osteosarcoma cell proliferation, which resembled the inhibitory effects of miR-23a overexpression. Taken together, our data provide compelling evidence that miR-23a functions as a tumor suppressor in osteosarcoma, and its inhibitory effect on tumor are mediated chiefly through downregulation of SATB1.
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页码:4715 / 4721
页数:7
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