JaLCDOI 10.18926/AMO/54982
フルテキストURL 71_2_135.pdf
著者 Mori, Akihiro| Watanabe, Masami| Sadahira, Takuya| Kobayashi, Yasuyuki| Ariyoshi, Yuichi| Ueki, Hideo| Wada, Koichiro| Ochiai, Kazuhiko| Li, Shun-Ai| Nasu, Yasutomo|
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 28420895
JaLCDOI 10.18926/AMO/32823
フルテキストURL fulltext.pdf
著者 Nakanishi, Akira| Kinuta, Keiko| Abe, Tadashi| Araki, Kenta| Yoshida, Yumi| Liang, Shuang| Li, Shun-Ai| Takei, Kohji| Kinuta, Masahiro|
抄録 <p>Administration of phenylhydrazine to rabbits resulted in the denaturation of hemoglobins in erythrocytes, causing the formation of intracellular precipitates known as Heinz bodies, severe hemolytic anemia, and reticulocytosis. To elucidate the molecular mechanism of the destabilization, we allowed human oxyhemoglobins to react aerobically with phenylhydrazine. After treatment with acetic acid/HCl and H2SO4/methanol, the chloroform extract contained blue-green pigments of major products accompanied by different minor products. Each product was isolated by column chromatography. By fast-atom-bombardment mass spectrometry (FAB-MS) and proton nuclear magnetic resonance (1H-NMR) spectrometry, dimethyl esters of N-phenylprotoporphyrin IX and meso, N-diphenylprotoporphyrin IX were determined. Other major products also were determined to be dimethyl esters of triphenyl-and tetraphenyl-substituted protoporphyrins by FAB-MS. The formation of meso, N-diphenylprotoporphyrin indicated that the addition of a phenyl radical to the meso-carbon atom of the protoporphyrin ring occurred. Triphenyl and tetraphenyl adducts also indicated the formation of phenyl radicals in the aerobic reaction of phenylhydrazine with oxyhemoglobins. From these results, we suggest that the formation of phenyl radicals and the replacement of heme with phenyl-substituted protoporphyrins cause the destabilization of hemoglobins to induce Heinz bodies and hemolytic anemia with phenylhydrazine.</p>
キーワード phenylhydrazine hemoglobin protoporphyrin fast-atom-bombardment mass spectrometry(FAB-MS) proton nuclear magnetic resonance(H-NMR)spectrometry
Amo Type Article
発行日 2003-10
出版物タイトル Acta Medica Okayama
57巻
5号
出版者 Okayama University Medical School
開始ページ 249
終了ページ 256
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
PubMed ID 14679403
Web of Sience KeyUT 000186186000006