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This article is part of the supplement: Twelfth International Conference on Bioinformatics (InCoB2013): Computational Biology

Open Access Research

Co-modulated behavior and effects of differentially expressed miRNA in colorectal cancer

Wei-Shone Chen1, Ting-Wen Chen23, Tzu-Hsien Yang4, Ling-Yueh Hu5, Hung-Wei Pan6, Chung-Man Leung7, Sung-Chou Li8, Meng-Ru Ho9, Chih-Wen Shu6, Pei-Feng Liu6, Shou-Yu Yu6, Ya-Ting Tu6, Wen-Chang Lin5, Tony T Wu1011* and Kuo-Wang Tsai6*

Author Affiliations

1 Department of Surgery, Veterans General Hospital, Taipei, Taiwan

2 Molecular Medicine Research Center, Chang Gung University, Taoyuan, Taiwan

3 Bioinformatics Center, Chang Gung University, Taoyuan, Taiwan

4 Department of Biotechnology and Laboratory Science in Medicine and Institute of Biotechnology in Medicine, National Yang Ming University, Taipei, Taiwan

5 Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan

6 Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan

7 Department of Radiation Oncology, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan

8 Clinical Genomics & Proteomics Core Laboratory, Department of medical research, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan

9 Genomics Research Center, Academia Sinica, Taipei, Taiwan

10 Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan

11 School of Medicine, Yang-Ming University, Taipei, Taiwan

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BMC Genomics 2013, 14(Suppl 5):S12  doi:10.1186/1471-2164-14-S5-S12

Published: 16 October 2013

Abstract

Background

MicroRNAs (miRNAs) are short noncoding RNAs (approximately 22 nucleotides in length) that play important roles in colorectal cancer (CRC) progression through silencing gene expression. Numerous dysregulated miRNAs simultaneously participate in the process of colon cancer development. However, the detailed mechanisms and biological functions of co-expressed miRNA in colorectal carcinogenesis have yet to be fully elucidated.

Results

The objective of this study was to identify the dysfunctional miRNAs and their target mRNAs using a wet-lab experimental and dry-lab bioinformatics approach. The differentially expressed miRNA candidates were identified from 2 miRNA profiles, and were confirmed in CRC clinical samples using reported target genes of dysfunctional miRNAs to perform functional pathway enrichment analysis. Potential target gene candidates were predicted by an in silico search, and their expression levels between normal and colorectal tumor tissues were further analyzed using real-time polymerase chain reaction (RT-PCR).

We identified 5 miRNAs (miR-18a, miR-31, miR-96, miR-182, and miR-224) and 10 miRNAs (miR-1, miR-9, miR-10b, miR-133a, miR-143, miR-137, miR-147b, miR-196a/b, and miR-342) that were significantly upregulated and downregulated in colon tumors, respectively. Bioinformatics analysis showed that the known targets of these dysregulated miRNAs simultaneously participated in epithelial-to-mesenchymal transition (EMT), cell growth, cell adhesion, and cell cycles. In addition, we identified that several pivotal target gene candidates may be comodulated by dysfunctional miRNAs during colon cancer progression. Finally, 7 candidates were proven to be differentially expressed, and had an anti-correlationship with dysregulated miRNA in 48 CRC samples.

Conclusion

Fifteen dysfunctional miRNAs were engaged in metastasis-associated pathways through comodulating 7 target genes, which were identified by using a multi-step approach. The roles of these candidate genes are worth further exploration in the progression of colon cancer, and could potentially be targets in future therapy.

Keywords:
microRNA; colorectal cancer; pathway enrichment analysis