Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2017 (2017), Article ID 2769140, 7 pages
https://doi.org/10.1155/2017/2769140
Research Article

Screening of Tumor Suppressor Genes in Metastatic Colorectal Cancer

1Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China
2Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China

Correspondence should be addressed to Yanqing Ding

Received 6 December 2016; Accepted 16 February 2017; Published 4 April 2017

Academic Editor: Kevin M. Coombs

Copyright © 2017 Lu Qi and Yanqing Ding. 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.

Abstract

Most tumor suppressor genes are commonly inactivated in the development of colorectal cancer (CRC). The activation of tumor suppressor genes may be beneficial to suppress the development and metastasis of CRC. This study analyzed genes expression and methylation levels in different stages of CRC. Genes with downregulated mRNA expression and upregulated methylation level in advanced CRC were screened as the potential tumor suppressor genes. After comparing the methylation level of screened genes, we found that MBD1 gene had downregulated mRNA expression and upregulated methylation levels in advanced CRC and continuously upregulated methylation level in the progression of CRC. Enrichment analysis revealed that genes expression in accordance with the elevated expression of MBD1 mainly located on chromosomes 17p13 and 17p12 and 8 tumor suppressor genes located on chromosome 17p13. Further enrichment analysis of transcription factor binding site identified that SP1 binding site had higher enrichment and could bind with MBD1. In conclusion, MBD1 may be a tumor suppressor gene in advanced CRC and affect the development and metastasis of CRC by regulating 8 tumor suppressor genes through binding with SP1.