期刊论文详细信息
Diagnostic Pathology
Hypermethylation of EDNRB promoter contributes to the risk of colorectal cancer
Shiwei Duan4  Meng Ye2  Leiting Xu4  Fei Chen4  Huadan Ye4  Yi Huang3  Qi Liao4  Lingyan Wang1  Cheng Chen2 
[1] Bank of Blood Products, Ningbo No.2 Hospital, Ningbo, Zhejiang 315010, China;The Affiliated Hospital, Ningbo University, Ningbo, Zhejiang 315000, China;Department of Neurosurgery, Ningbo First Hospital, Ningbo University, Ningbo, Zhejiang 315010, China;Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, Zhejiang 315211, China
关键词: Biomarker;    DNA methylation;    EDNRB;    Colorectal cancer;   
Others  :  803826
DOI  :  10.1186/1746-1596-8-199
 received in 2013-10-22, accepted in 2013-12-06,  发布年份 2013
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【 摘 要 】

Objective

Colorectal cancer (CRC) is one of the most common digestive malignancies in the world. EDNRB is a new candidate tumor suppressor gene which is often down-regulated or even silenced by promoter hypermethylation in various human cancers. However, the function of EDNRB gene in CRC remains unknown. In this study, we examined the expression and DNA methylation of EDNRB in CRC tissues.

Methods

A total of 42 paired CRC and adjacent normal tissue samples were used to determine mRNA levels and DNA methylation status of EDNRB gene by qRT-PCR and methylation-specific PCR (MSP), respectively.

Results

Our study showed that EDNRB promoter hypermethylation was more frequently in CRC tissues than in the normal tissues (92.86 versus 59.52, p = 0.001). Consequently, significantly lower level of EDNRB mRNA was found in CRC tumor samples than in normal samples (0.31 ± 0.91 versus 0.70 ± 1.18, p = 0.032).

Conclusions

Our results suggested that EDNRB promoter hypermethylation might downregulate its gene expression in CRC, and thus played an important role in the development of CRC.

The virtual slide

The virtual slides for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/7420980471113303 webcite

【 授权许可】

   
2013 Chen et al.; licensee BioMed Central Ltd.

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