MicroRNA-25 functions as a potential tumor suppressor in colon cancer by targeting Smad7

被引:160
作者
Li, Qiang [2 ]
Zou, Chaoxia [1 ]
Zou, Chendan [1 ]
Han, Zhongjing [1 ]
Xiao, Haifeng [1 ]
Wei, Huiyan [1 ]
Wang, Wei [1 ]
Zhang, Lei [1 ]
Zhang, Xueying [1 ]
Tang, Qingchao [2 ]
Zhang, Chunjing [4 ]
Tao, Ji [3 ]
Wang, Xishan [2 ]
Gao, Xu [1 ,5 ]
机构
[1] Harbin Med Univ, Dept Biochem & Mol Biol, Harbin, Peoples R China
[2] Harbin Med Univ, Affiliated Hosp 2, Dept Gen Surg, Harbin, Peoples R China
[3] Harbin Med Univ, Affiliated Hosp 3, Dept Med Oncol, Harbin, Peoples R China
[4] Qiqihar Med Univ, Dept Biochem & Mol Biol, Qiqihar, Peoples R China
[5] Minist Educ, Key Lab Cardiovasc Med Res, Harbin, Peoples R China
基金
中国博士后科学基金;
关键词
Colon cancer; MicroRNA-25; Smad7; Migration; Proliferation; IDENTIFICATION; EXPRESSION; REGULATOR; CLUSTERS;
D O I
10.1016/j.canlet.2013.02.029
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Because it is a member of the miR-106b similar to 25 cluster, microRNA-25 (miR-25) is known to be dysregulated in human cancers. However, the expression and role of miR-25 in colon cancer remain unclear. In this study, miR-25 was found to be down-regulated in human colon cancer tissues when compared to those in matched, non-neoplastic mucosa tissues. Functional studies revealed that restoration of miR-25 expression inhibited cell proliferation and migration. In contrast, miR-25 inhibition could promote the proliferation and migratory ability of cells. Stable over-expression of miR-25 also suppressed the growth of colon cancer-cell xenografts in vivo. Furthermore, bioinformatic predictions and experimental validation were used to identify Smad7 as a direct target of miR-25. Functional reverse experiments indicated that the antitumor effects of miR-25 were probably mediated by its repression of Smad7. These results suggest that miR-25 may function as a tumor suppressor by targeting Smad7 in colon cancer. Thus, miR-25 may serve as a potential therapeutic agent or target for cancer therapy. Crown Copyright (c) 2013 Published by Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:168 / 174
页数:7
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