| Literature DB >> 23435373 |
Qiang Li1, Chaoxia Zou, Chendan Zou, Zhongjing Han, Haifeng Xiao, Huiyan Wei, Wei Wang, Lei Zhang, Xueying Zhang, Qingchao Tang, Chunjing Zhang, Ji Tao, Xishan Wang, Xu Gao.
Abstract
Because it is a member of the miR-106b~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. CrownEntities:
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Year: 2013 PMID: 23435373 DOI: 10.1016/j.canlet.2013.02.029
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679