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Disease Markers
Volume 2015 (2015), Article ID 345080, 7 pages
Research Article

Hypermethylation-Associated Silencing of miR-125a and miR-125b: A Potential Marker in Colorectal Cancer

1Department of Gastroenterology, People’s Hospital of Taizhou, 399 Hailing Road, Taizhou, Jiangsu 225300, China
2Department of Gastroenterology, Second Xiangya Hospital, Central South University, 139 Renmin Middle Road, Changsha, Hunan 410011, China

Received 5 September 2015; Revised 11 November 2015; Accepted 12 November 2015

Academic Editor: Stamatios Theocharis

Copyright © 2015 Hui Chen and Zhiying Xu. 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.


Background. MicroRNAs (miRNAs) have been found to be downregulated in human colorectal cancer (CRC), and some of them may function as tumor suppressor genes (TSGs). Aberrant methylation triggers the inactivation of TSGs during tumorigenesis. Patients and Methods. We investigated the methylation status of miR-125 family in CRC tissues and adjacent nontumor tissues by using bisulfite sequencing PCR (BSP). The expression levels of the two miRNAs were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results. The methylation frequency of miR-125a and miR-125b was higher in CRC tissues. QRT-PCR analysis showed that miR-125a and miR-125b were significantly downregulated in CRC tissues. Moreover, the expression levels of miR-125a and miR-125b were inversely correlated to CpG island methylation in CRC. Conclusions. Our results suggest that DNA hypermethylation may be involved in the inactivation of miR-125a and miR-125b in CRC, and hypermethylation of miR-125 is a potential biomarker for clinical outcome.