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• W2214095296 abstract "// Jong-Lyul Park 1,2,* , Hee-Jin Kim 1,2,* , Eun-Hye Seo 1,2 , Oh-Hyung Kwon 1 , Byungho Lim 1 , Mirang Kim 1,2 , Seon-Young Kim 1,2 , Kyu-Sang Song 3 , Gyeong Hoon Kang 4 , Hyun Ja Kim 5 , Bo Youl Choi 5 and Yong Sung Kim 1,2 1 Epigenome Research Center, Genome Institute, KRIBB, Daejeon, Republic of Korea 2 Department of Functional Genomics, Korea University of Science and Technology, Daejeon, Republic of Korea 3 Department of Pathology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea 4 Department of Pathology, Seoul National University College of Medicine, Seoul, Republic of Korea 5 Departments of Preventive Medicine, College of Medicine, Hanyang University, Seoul, Republic of Korea * These authors have contributed equally to this work Correspondence to: Yong Sung Kim, email: // Keywords : gastric cancer, TET1, DNA methylation, 5-hydroxymethylcytosine, 3′-shore, bivalent mark Received : May 10, 2015 Accepted : September 26, 2015 Published : October 10, 2015 Abstract Recent evidence has shown that the level of 5-hydroxymethylcytosine (5hmC) in chromosomal DNA is aberrantly decreased in a variety of cancers, but whether this decrease is a cause or a consequence of tumorigenesis is unclear. Here we show that, in gastric cancers, the 5hmC decrease correlates with a decrease in ten-eleven translocation 1 ( TET 1) expression, which is strongly associated with metastasis and poor survival in patients with gastric cancer. In gastric cancer cells, TET 1-targeted siRNA induced a decrease in 5hmC, whereas TET 1 overexpression induced an increase in 5hmC and reduced cell proliferation, thus correlating decreased 5hmC with gastric carcinogenesis. We also report the epigenetic signatures responsible for regulating TET 1 transcription. Methyl-CpG Binding Domain Sequencing and Reduced Representation Bisulfite Sequencing identified unique CpG methylation signatures at the CpG island 3′-shore region located 1.3 kb from the transcription start site of TET 1 in gastric tumor cells but not in normal mucosa. The luciferase activity of constructs with a methylated 3′-shore sequence was greatly decreased compared with that of an unmethylated sequence in transformed gastric cancer cells. In gastric cancer cells, dense CpG methylation in the 3′-shore was strongly associated with TET 1 silencing and bivalent histone marks. Thus, a decrease in 5hmC may be a cause of gastric tumorigenesis owing to a decrease in TET 1 expression through DNA methylation coupled with bivalent marks in the 3′-shore of TET 1." @default.
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• W2214095296 date "2015-10-10" @default.
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• W2214095296 title "Decrease of 5hmC in gastric cancers is associated with<i>TET1</i>silencing due to with DNA methylation and bivalent histone marks at<i>TET1</i>CpG island 3′-shore" @default.
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• W2214095296 doi "https://doi.org/10.18632/oncotarget.6069" @default.
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