このエントリーをはてなブックマークに追加
ID 54982
JaLCDOI
フルテキストURL
Thumnail 71_2_135.pdf 2.79 MB
著者
Mori, Akihiro Department of Urology, Okayama University, Graduate School of Medicine, Denistry and Pharmacentical Sciences
Watanabe, Masami Department of Urology, Okayama University, Graduate School of Medicine, Denistry and Pharmacentical Sciences
Sadahira, Takuya Department of Urology, Okayama University, Graduate School of Medicine, Denistry and Pharmacentical Sciences
Kobayashi, Yasuyuki Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Kaken ID
Ariyoshi, Yuichi Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Ueki, Hideo Department of Urology, Okayama University, Graduate School of Medicine, Denistry and Pharmacentical Sciences
Wada, Koichiro Department of Urology, Okayama University, Graduate School of Medicine, Denistry and Pharmacentical Sciences
Ochiai, Kazuhiko Department of Veterinary Nursing and Technology, Nippon Veterinary and Life Science University
Li, Shun-Ai Center for Innovative Clinical Medicine, Okayama University Hospital
Nasu, Yasutomo Department of Urology, Okayama University, Graduate School of Medicine, Denistry and Pharmacentical Sciences Kaken ID researchmap
抄録
The cluster of differentiation 147 (CD147), also known as EMMPRIN, is a key molecule that promotes cancer progression. We previously developed an adenoviral vector encoding a tumor suppressor REIC/Dkk-3 gene (Ad-REIC) for cancer gene therapy. The therapeutic effects are based on suppressing the growth of cancer cells, but, the underlying molecular mechanism has not been fully clarified. To elucidate this mechanism, we investigated the effects of Ad-REIC on the expression of CD147 in LNCaP prostate cancer cells. Western blotting revealed that the expression of CD147 was significantly suppressed by Ad-REIC. Ad-REIC also suppressed the cell growth of LNCaP cells. Since other researchers have demonstrated that phosphorylated mitogen-activated protein kinases (MAPKs) and c-Myc protein positively regulate the expression of CD147, we investigated the correlation between the CD147 level and the activation of MAPK and c-Myc expression. Unexpectedly, no positive correlation was observed between CD147 and its possible regulators, suggesting that another signaling pathway was involved in the downregulation of CD147. This is the first study to show the downregulation of CD147 by Ad-REIC in prostate cancer cells. At least some of the therapeutic effects of Ad-REIC may be due to the downregulation of the cancer-progression factor, CD147.
キーワード
prostate cancer
REIC/Dkk-3
CD147
cell growth
p38 MAP kinase
Amo Type
Original Article
発行日
2017-04
出版物タイトル
Acta Medica Okayama
71巻
2号
出版者
Okayama University Medical School
開始ページ
135
終了ページ
142
ISSN
0386-300X
NCID
AA00508441
資料タイプ
学術雑誌論文
言語
English
著作権者
CopyrightⒸ 2017 by Okayama University Medical School
論文のバージョン
publisher
査読
有り
PubMed ID