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

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• 作者：Qiang Li^b ; ¹ ; Chaoxia Zou^a ; ¹ ; Chendan Zou^a ; ¹ ; Zhongjing Han^a ; Haifeng Xiao^a ; Huiyan Wei^a ; Wei Wang^a ; Lei Zhang^a ; Xueying Zhang^a ; Qingchao Tang^b ; Chunjing Zhang^d ; Ji Tao^c ; Xishan Wang^b ; ^{wxshan1208@yahoo.com.cn} ; Xu Gao^a ; ^e ; ^{Gaoxu_671227@yahoo.com.cn}
• 关键词：Colon cancer ; MicroRNA-25 ; Smad7 ; Migration ; Proliferation
• 刊名：Cancer Letters
• 出版年：2013
• 出版时间：10 July, 2013
• 年：2013
• 卷：335
• 期：1
• 页码：168-174
• 全文大小：1389 K

文摘

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.