alexa CDH13 is Frequently Inactivated by Promoter Hypermethylation in Pediatric Acute Myeloid Leukemia (AML)
ISSN: 2329-8790

Journal of Hematology & Thromboembolic Diseases
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Research Article

CDH13 is Frequently Inactivated by Promoter Hypermethylation in Pediatric Acute Myeloid Leukemia (AML)

Tao Yan-Fang1, Feng Xing1, Wang Jian1, Zhao Wen-Li1, Xiao-Juan Du2, Wu Shui-Yan1, Wang Na1, Hu Shao-Yan1, Cao Lan1, Li Yan-Hong1, MD, Ni Jian3, MD, and Pan Jian1*

1Department of Hematology and Oncology, Children’s Hospital of Soochow University, Suzhou, China

2Department of Gastroenterology, The 5th Hospital of Chinese PLA, Yin Chuan, Ningxia Province, China

3Translational Research Center, Second Hospital, The Second Clinical School, Nanjing Medical University, Nanjing, China

*Corresponding Author:
Pan Jian
Associate professor
Department of Hematology and Oncology
Children’s Hospital of Soochow University
Suzhou, China
Tel: (86)512-67788216
Fax: (86)512-67788216
E-mail: [email protected]

Received March 15, 2013; Accepted April 23, 2013; Published April 26, 2013

Citation: Yan-Fang T, Xing F, Jian W, Wen-Li Z, Du XJ, et al. (2013) CDH13 is Frequently Inactivated by Promoter Hypermethylation in Pediatric Acute Myeloid Leukemia (AML). J Hematol Thromb Dis 1:111. doi:10.4172/2329-8790.1000111

Copyright: © 2013 Yan-Fang T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

There is growing evidence supporting a role for tumor suppressor as targets in aberrant mechanisms of DNA hypermethylation. Methylation in the promoter of tumor suppressor always plays important roles in pediatric Acute Myeloid Leukemia (AML). CDH13 gene is a tumor suppressor involved in tumorigenesis, metastasis and apoptosis in a variety of tumors. In this study, we are trying to investigate whether CDH13 was down regulated by promoter methylation in pediatric AML. MRNA transcriptional expression levels of CDH13 were evaluated by semi-quantitative PCR and real-time PCR. Methylation status of CDH13 prompter was investigated by Methylation Specific PCR (MSP) and Bisulfate Genomic Sequencing (BGS). CDH13 mRNA transcription was inactivated in AML cell lines. Promoter of CDH13 was aberrantly methylated in 55.6% (5/9) leukemia cell lines. Promoter aberrant methylation of CDH13 was detected in 34.2% (24/70) of the cases of pediatric AML. The methylation of CDH13 promoter could be detected in all FAB subtypes. There were no significant differences in clinical features between patients with and without CDH13 methylation. Expression of CDH13 was significantly lower in AML patients group compared to normal bone marrow (NBM) control samples .The expression of CDH13 in thirty controls was significantly higher than pediatric AML patients. Both patients with CDH13 methylation (n=24) and those without CDH13 methylation (n=46) had significantly lower CDH13 transcript than controls (p<0.001). CDH13 transcript was significantly lower in patients with methylated CDH13 than those without methylated CDH13 (p=0.036). Inactivation of CDH13 by promoter hypermethylation is frequent event in pediatric AML. Our results suggest that hypermethylation of CDH13 promoter might be one of early events in the development of pediatric AML.

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