miR-34a inhibits the in vitro cell proliferation and migration in human esophageal cancer

被引：30
作者：
Shi, Hui [1 ,2 ,3 ]
Zhou, Shengluan [1 ]
Liu, Junhua [1 ]
Zhu, Jun [1 ]
Xue, Jianhua [1 ]
Gu, Luo [2 ]
Chen, Yijiang [3 ]
机构：
[1] Nantong Univ, Affiliated Hosp, Dept Cardiothorac Surg, Nantong City 226001, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Dept Biochem & Mol Biol, Nantong City 210000, Jiangsu, Peoples R China
[3] Nanjing Med Univ, Affiliated Hosp 1, Dept Thorac Surg, Nantong City 210000, Jiangsu, Peoples R China
来源：
PATHOLOGY RESEARCH AND PRACTICE | 2016年 / 212卷 / 05期
关键词：
miR-34a; Human esophageal cancer; DNA methylation; p53; TUMOR-SUPPRESSOR; CARCINOMA CELLS; DOWN-REGULATION; C-MET; APOPTOSIS; MICRORNA; INVASION; EXPRESSION; PATHWAY; GROWTH;
D O I：
10.1016/j.prp.2016.02.019
中图分类号：
R36 [病理学];
学科分类号：
100104 ;
摘要：
Background: Increasing studies demonstrate that reduced expression of miR-34a is involved in the initiation and progression of cancers, and it has been characterized as a tumor suppressor in various types of cancers. In present study, we investigated the expression and role of miR-34a in esophageal cancer. Methods: qRT-PCR assays were performed to analyze the expression of miR-34a in human esophageal cancer tissues and adjacent esophageal tissues. CCK8 assay, flow cytometry analysis and in vitro migration assays were performed to analyze the role of miR-34a in human esophageal cancer cell. MSP assay was performed to analyze the DNA methylation of the miR-34a promoter. Results: The expression of miR-34a was down-regulated in human esophageal cancer tissues. miR-34a ectopic expression affected esophageal cancer cells survival, proliferation and capabilities of migration in vitro. p53 status was not correlated with miR-34a. Subsequently, aberrant DNA methylation of the miR-34a promoter was found in human esophageal cancer, and 5-AZA-dC inhibited DNA methylation of the miR-34a promoter. Conclusions: our data showed that miR-34a acted as a tumor suppressor in human esophageal cancer. (C) 2016 Published by Elsevier GmbH.
引用
收藏
页码：444 / 449
页数：6
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