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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
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
Abstract
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.
Keywords
prostate cancer
REIC/Dkk-3
CD147
cell growth
p38 MAP kinase
Amo Type
Original Article
Published Date
2017-04
Publication Title
Acta Medica Okayama
Volume
volume71
Issue
issue2
Publisher
Okayama University Medical School
Start Page
135
End Page
142
ISSN
0386-300X
NCID
AA00508441
Content Type
Journal Article
language
英語
Copyright Holders
CopyrightⒸ 2017 by Okayama University Medical School
File Version
publisher
Refereed
True
PubMed ID