An association between overexpression of DNA methyltransferase 3B4 and clear cell renal cell carcinoma
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You Liu1, Liantao Sun1, Peter Fong2, Jie Yang1, Zhuxia Zhang1, Shuihui Yin1, Shuyuan Jiang1, Xiaolei Liu1, Hongge Ju1, Lihua Huang1, Jing Bai1, Kerui Gong3, Shaochun Yan1, Chunyang Zhang4, Guo Shao1,5
1Biomedicine Research Center and Basic Medical College, Baotou Medical College, Inner Mongolia, PRC
2Department of Neurology, University of California San Francisco, San Francisco, CA, USA
3Department of Oral and Maxillofacial Surgery, University of California San Francsico, San Francisco, CA, USA
4Department of Neurology, First Affiliated Hospital of Baotou Medical College, Inner Mongolia, PRC
5Institute for Hypoxia Medicine, Capital Medical University, Beijing, PRC
Chunyang Zhang, email: [email protected]
Guo Shao, email: [email protected]
Keywords: DNA methyltransferase 3B, clear cell renal cell carcinoma
Received: June 07, 2016 Accepted: January 03, 2017 Published: February 01, 2017
It is well known that abnormal DNA methylations occur frequently in kidney cancer. However, it remains unclear exactly which types of DNA methyltransferases (DNMT) contribute to the pathologies of kidney cancers. In order to determine the functions of DNA methyltransferase in kidney tumorigenesis on the molecular level, we examined the mRNA expression levels of DNMT1, DNMT3A, DNMT3B, and DNMT3B variants in renal cell carcinoma tissue. Both mRNA and protein levels of DNMT3B4, a splice variant of DNMT3B, were increased in renal cell carcinoma tissue compared with adjacent control tissues. Additionally, Alu elements and long interspersed nuclear elements (LINE-1) were hypomethylated in renal cell carcinoma tissue. Meanwhile, methylation of the promoter for RASSF1A, a tumor suppressor gene, was moderately increased in renal cell carcinoma tissue, while RASSF1A expression was decreased. Thus, our data suggest that the overexpression of DNMT3B4 may play an important role in human kidney tumorigenesis through chromosomal instability and methylation of RASSF1A.
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