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KAKEN_26462429seika.pdf
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Title |
Title |
尿路上皮癌における抗がん剤耐性獲得下の微小環境とユビキチンシステムの解明
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Kana |
ニョウロ ジョウヒガン ニ オケル コウガンザイ タイセイ カクトクカ ノ ビショウ カンキョウ ト ユビキチン システム ノ カイメイ
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Nyoro johigan ni okeru koganzai taisei kakutokuka no bisho kankyo to yubikichin shisutemu no kaimei
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Tumor microenvironment and ubiquitin system in platinum resistance urothelial carcinoma
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田中, 伸之
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Kana |
タナカ, ノブユキ
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Romanization |
Tanaka, Nobuyuki
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Affiliation |
慶應義塾大学・医学部・講師(非常勤)
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Research team head
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科研費研究者番号 : 60445244
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小坂, 威雄
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Kana |
コサカ, タケオ
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Romanization |
Kosaka, Takeo
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Affiliation |
慶應義塾大学・医学部・講師
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Research team member
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科研費研究者番号 : 30445407
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大家, 基嗣
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オオヤ, モトツグ
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Oya, Mototsugu
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慶應義塾大学・医学部・教授
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Research team member
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科研費研究者番号 : 00213885
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松本, 一宏
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Kana |
マツモト, カズヒロ
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Matsumoto, Kazuhiro
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慶應義塾大学・医学部・助教
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Research team member
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科研費研究者番号 : 80366153
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丹羽, 直也
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ニワ, ナオヤ
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Niwa, Naoya
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慶應義塾大学・医学部・助教
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Research team member
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科研費研究者番号 : 40626743
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2017
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科学研究費補助金研究成果報告書
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2016
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Abstract |
シスプラチン(CDDP)治療後の再燃性尿路上皮癌では上皮間葉転換(EMT)が治療標的となり得る。我々はCDDP耐性尿路上皮癌T24PR・5637PR細胞のアレイ解析から, CDDP耐性下のFBXO32発現低下に注目した。In vitroではFBXO32ノックダウンに伴うEMT誘導が確認され, 結果は過剰発現系で検証された。臨床組織ではFBXO32低発現群におけるEMT誘導が確認された。FBXO32発現低下の原因として, T24PR細胞ではFBXO32遺伝子のコード領域でヘテロ接合性消失が確認された。5637PR細胞ではFOXO1/3aの核内発現が低下しており, FBXO32発現抑制の一因と考えられた。
To identify the molecules involved in epithelial-to-mesenchymal transition (EMT) in tumors post acquired platinum resistance (PR), we examined the changes in gene expression before and after platinum treatment. Four urothelial carcinoma cell lines, T24, 5637, and their PR sublines of T24PR and 5637PR, were assessed by microarray, and FBXO32 was newly identified as a negative regulator of EMT. In vitro study showed an intimate relationship between FBXO32 expression and EMT, demonstrating that FBXO32 knockdown resulted in the EMT acquisition. In contract, FBXO32 overexpression suppressed EMT. The association between FBXO32 expression and EMT was further validated using human specimens. CGH array analysis demonstrated loss of heterozygosity at 8q24.13 in T24PR cells, which harbors FBXO32. In 5637PR cells, decreased nuclear FOXO1/3a expression seemed to affect FBXO32 dysregulation. These results suggest the association between EMT and ubiquitin-proteasome regulation when tumors develop PR.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2014~2016
課題番号 : 26462429
研究分野 : 泌尿器科学
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Nov 7, 2017 | | 概要, フリーキーワード, 抄録, 著者 を変更 |
Nov 8, 2017 | | 著者 を変更 |
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