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Disease Markers
Volume 2014 (2014), Article ID 617150, 11 pages
Research Article

MicroRNA-224 Suppresses Colorectal Cancer Cell Migration by Targeting Cdc42

1Institute of Medicine, Chung-Shan Medical University, Taichung 402, Taiwan
2Division of Colorectal Surgery, Department of Surgery, China Medical University Hospital, Taichung 404, Taiwan
3Department of Internal Medicine, Taipei Medical University-Wan Fang Hospital, Taipei 116, Taiwan
4Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
5PhD Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan
6Center for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan
7Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei 114, Taiwan

Received 7 November 2013; Revised 15 March 2014; Accepted 23 March 2014; Published 10 April 2014

Academic Editor: Valeria Barresi

Copyright © 2014 Tao-Wei Ke et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The metastatic spread of tumor cells is the major risk factor affecting the clinical prognosis of colorectal cancer (CRC) patients. The metastatic phenotype can be modulated by dysregulating the synthesis of different structural and functional proteins of tumor cells. Micro(mi)RNAs are noncoding RNAs that recognize their cognate messenger (m)RNA targets by sequence-specific interactions with the 3′ untranslated region and are involved in the multistep process of CRC development. The objective of this study was to investigate the expression and biological roles of miR-224 in CRC. The miR-224 expression level was assessed by a quantitative real-time PCR in 79 CRC and 18 nontumor tissues. Expression levels of miR-224 in CRC tissues were significantly lower than those in nontumor tissues. Its expression level was associated with the mutation status of the APC gene. Ectopic expression of miR-224 suppressed the migratory ability of CRC cell line, but cell proliferation was less affected. Increased miR-224 diminished Cdc42 and SMAD4 expressions at both the protein and mRNA levels and inhibited the formation of actin filaments. Overall, this study indicated a role of miR-224 in negatively regulating CRC cell migration. The expression level of miR-224 may be a useful predictive biomarker for CRC progression.