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ID 30945
JaLCDOI
フルテキストURL
著者
Kobayashi, Tomoko Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Sakaguchi, Masakiyo Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Tanimoto, Ryuta Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Abarzua, Fernando Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Takaishi, Mikiro Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kaku, Haruki Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kataoka, Ken Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Saika, Takashi Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Nasu, Yasutomo Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Miyazaki, Masahiro Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kumon, Hiromi Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Huh, Nam-ho Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
抄録

We have recently shown that a new therapeutic modality using the REIC/Dkk-3 gene (Ad-REIC) is effective against various human cancers, including those of prostate, testis and breast origins. The aim of the present study was to examine the sensitivity of bladder cancers to Ad-REIC and to clarify the molecular mechanisms that determine sensitivity/resistance. We found that 2 human bladder cancer cell lines, T24 and J82, are resistant to Ad-REIC. In T24 and J82 cells, the ER stress response and activation of JNK were observed in a manner similar to that in the sensitive PC3 cells. Translocation of Bax to mitochondria occurred in PC3 cells but not in T24 and J82 cells. Bcl-2 was remarkably overexpressed in T24 and J82 compared with the expression levels in sensitive cell lines. Treatment of T24 and J82 cells with a Bcl-2 inhibitor sensitized the cells to Ad-REIC-induced apoptosis. The results indicate that some human bladder cancers are resistant to apoptosis induced by overexpression of REIC/Dkk-3, which is at least in part due to up-regulation of Bcl-2. These results provide a basis for possible use of Bcl-2 as a marker of sensitive cancers and to try to sensitize resistant cancers to Ad-REIC by down-regulation of Bcl-2.

キーワード
REIC/Dkk-3
bladder cancer
apoptosis
Bcl-2
Amo Type
Original Article
発行日
2008-12
出版物タイトル
Acta Medica Okayama
62巻
6号
出版者
Okayama University Medical School
開始ページ
393
終了ページ
401
ISSN
0386-300X
NCID
AA00508441
資料タイプ
学術雑誌論文
言語
English
論文のバージョン
publisher
査読
有り
Web of Sience KeyUT