2013 Fiscal Year Final Research Report
Contribution of TET1 to malignant characteristics in digestive cancer cells.
Project/Area Number |
24790682
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Gastroenterology
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Research Institution | The University of Tokyo |
Principal Investigator |
KUDO Yotaro 東京大学, 医学部附属病院, 特任臨床医 (90608358)
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Project Period (FY) |
2012-04-01 – 2014-03-31
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Keywords | 肝臓学 |
Research Abstract |
Ten-Eleven-Translocation (TET) proteins mediate the conversion from 5-methylcytosine to 5-hydroxymethylcytosine (5-hmC), which is an intermediate of DNA demethylation. We aim to elucidate whether TET-mediated DNA demethylation is involved in biological properties in solid cancers. We have reported a loss of global 5-hmC level in a broad spectrum of human tumors. These findings suggest critical roles of abnormal DNA demethylation for oncogenic processes in solid tissues. Next, we focus on the role of TET1 protein in cancers, especially gastrointestinal and hepatic cancers. We found that TET1-depletion suppressed cell proliferation in various cell lines, and gene expression array analysis was carried out to validate responsible genes.
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[Presentation] Contribution of TET1 to malignant characteristics in digestive cancer cells2013
Author(s)
Yotaro Kudo, Keisuke Tateishi, Tsuneo Ikenoue, Keisuke Yamamoto, Shinzo Yamamoto, Yoshinari Asaoka, Hideaki Ijichi, Genta Nagae, Masato Yonezawa, Motoaki Seki, Kiyokazu Shirai, Haruhiko Yoshida, Hiroyuki Aburatani, Kazuhiko Koike
Organizer
Cell Symposia: Cancer Epigenomics
Place of Presentation
Sitges, Spain
Year and Date
20131006-08
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