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.
引用
收藏
页码:4715 / 4721
页数:7
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