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Author Tang, Qingchao ♦ Zou, Zhaoxia ♦ Zou, Chendan ♦ Zhang, Qian ♦ Huang, Rui ♦ Guan, Xu ♦ Li, Qiang ♦ Han, Zhongjing ♦ Wang, Dayong ♦ Wei, Huiyan ♦ Gao, Xu ♦ Wang, Xishan
Source SpringerLink
Content type Text
Publisher Springer Netherlands
File Format PDF
Copyright Year ©2014
Language English
Subject Domain (in DDC) Technology ♦ Medicine & health
Subject Keyword Colorectal cancer ♦ MicroRNA-93 ♦ Wnt/β-catenin ♦ Invasion ♦ Proliferation ♦ Cancer Research
Abstract MicroRNA-93 (miR-93) is involved in several carcinoma progressions. It has been reported that miR-93 acts as a promoter or suppressor in different tumors. However, till now, the role of miR-93 in colon cancer is unclear. Herein, we have found that expression of miR-93 was lower in human colon cancer tissue and colorectal carcinoma cell lines compared with normal colon mucosa. Forced expression of miR-93 in colon cancer cells inhibits colon cancer invasion, migration, and proliferation. Furthermore, miR-93 may downregulate the Wnt/β-catenin pathway, which was confirmed by measuring the expression level of the β-catenin, axin, c-Myc, and cyclin-D1 in this pathway. Mothers against decapentaplegic homolog 7 (Smad7), as an essential molecular protein for nuclear accumulation of β-catenin in the canonical Wnt signaling pathway, is predicted as a putative target gene of miR-93 by the silico method and demonstrated that it may be suppressed by targeting its 3′UTR. These findings showed that miR-93 suppresses colorectal cancer development via downregulating Wnt/β-catenin, at least in part, by targeting Smad7. This study revealed that miR-93 is an important negative regulator in colon cancer and suggested that miR-93 may serve as a novel therapeutic agent that offers benefits for colon cancer treatment.
ISSN 10104283
Age Range 18 to 22 years ♦ above 22 year
Educational Use Research
Education Level UG and PG
Learning Resource Type Article
Publisher Date 2014-11-05
Publisher Place Dordrecht
e-ISSN 14230380
Journal Tumor Biology
Volume Number 36
Issue Number 3
Page Count 10
Starting Page 1701
Ending Page 1710

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Source: SpringerLink