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  1. 教員研究業績
  2. 臨床薬剤学研究室
  3. 原著論文

Ten-eleven translocation 1 functions as a mediator of SOD3 expression in human lung cancer A549 cells.

https://gifu-pu.repo.nii.ac.jp/records/13180
https://gifu-pu.repo.nii.ac.jp/records/13180
fe2c6209-def2-4eab-bbdb-05d2987499cd
Item type 研究室原著論文(1)
公開日 2018-06-14
タイトル
タイトル Ten-eleven translocation 1 functions as a mediator of SOD3 expression in human lung cancer A549 cells.
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
抄録
値 Superoxide dismutase (SOD) 3, one of the SOD isozymes, plays a pivotal role in extracellular redox homeostasis. The expression of SOD3 is regulated by epigenetics in human lung cancer A549 cells and human monocytic THP-1 cells; however, the molecular mechanisms governing SOD3 expression have not been elucidated in detail. Ten-eleven translocation (TET), a dioxyge- nase of 5-methylcytosine (5mC), plays a central role in DNA demethylation processes and induces target gene expression. In the present study, TET1 expression was abundant in U937 cells, but its expression was weakly expressed in A549 and THP-1 cells. These results are consistent with the expression pattern of SOD3 and its DNA methylation status in these cells. Moreover, above rela- tionship was also observed in human breast cancer cells, human prostate cancer cells, and human skin fibroblasts. The overexpression of TET1-catalytic domain (TET1-CD) induced the expression of SOD3 in A549 cells, and this was accompanied by the direct binding of TET1-CD to the SOD3 promoter region. Furthermore, in TET1-CD-transfected A549 cells, the level of 5-hydrox- ymethylcytosine within that region was significantly increased, whereas the level of 5mC was decreased. The results of the present study demonstrate that TET1 might function as one of the key molecules in SOD3 expression through its 5mC hydroxylation in A549 cells.
書誌情報 en : Free radical research

巻 51, 号 3, p. 329-336, 発行日 2017-03
DOI
値 10.1080/10715762.2017.1313415
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