MicroRNA-204 suppressed proliferation and motility capacity of human hepatocellular carcinoma via directly targeting zinc finger E-box binding homeobox 2

被引:13
作者
Hu, Bin [1 ]
Sun, Ming [2 ]
Liu, Jiajun [3 ]
Hong, Guolin [1 ]
Lin, Qin [4 ]
机构
[1] Xiamen Univ, Affiliated Hosp 1, Dept Lab Med, 55 Zhenhai Rd, Xiamen 361003, Fujian, Peoples R China
[2] Xiamen Univ, Affiliated Hosp 1, Dept Reprod Med, Xiamen 361003, Fujian, Peoples R China
[3] Xiamen Univ, Affiliated Hosp 1, Dept Infect Dis, Xiamen 361003, Fujian, Peoples R China
[4] Xiamen Univ, Affiliated Hosp 1, Dept Radiat Oncol, 55 Zhenhai Rd, Xiamen 361003, Fujian, Peoples R China
基金
中国国家自然科学基金;
关键词
microRNA-204; zinc finger F-box binding homeobox 2; proliferation; metastasis; motility; hepatocellular carcinoma; INHIBITS CELL-PROLIFERATION; EPITHELIAL-MESENCHYMAL TRANSITION; POOR-PROGNOSIS; UP-REGULATION; MIGRATION; INVASION; CANCER; EXPRESSION; MIR-204; ZEB2;
D O I
10.3892/ol.2017.5907
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Abnormal expression levels of microRNA-204 (miR-204) have been identified in various types of human cancer. However, the expression and functions of miR-204, and the underlying molecular mechanism involved in the initiation and progression of hepatocellular carcinoma (HCC), require further investigation. The results of the present study demonstrated that miR-204 is downregulated in HCC tissues and cell lines. Notably, zinc finger E-box binding homeobox 2 (ZEB2) was identified as a direct target of miR-204 in HCC. In addition, miR-204 negatively regulates ZEB2 expression level in HCC cells at the post-transcriptional level. In functional studies, the overexpression of miR-204 inhibited the proliferation, migration and invasion of HCC cells. Furthermore, the knockdown of ZEB2 may mimic the functions of miR-204 in HCC cells, suggesting that ZEB2 is a direct functional target of miR-204. In conclusion, the results of the present study indicated that miR-204 suppresses the tumor growth, migration and invasion of HCC cells by directly targeting ZEB2, and may serve as a novel therapeutic target for HCC.
引用
收藏
页码:3823 / 3830
页数:8
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