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KAKEN_25513008seika.pdf
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Title |
Title |
メチオニン代謝の可視化によるがん進展におけるエピゲノム制御機構の解明
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Kana |
メチオニン タイシャ ノ カシカ ニ ヨル ガン シンテン ニ オケル エピゲノム セイギョ キコウ ノ カイメイ
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Mechionin taisha no kashika ni yoru gan shinten ni okeru epigenomu seigyo kiko no kaimei
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Analysis of epigenetic regulation by visualizing S-adenosylmethionine metabolism in cancer cells using imaging mass spectrometry.
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久保, 亜紀子
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クボ, アキコ
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Kubo, Akiko
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Affiliation |
慶應義塾大学・医学部・特任講師
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Research team head
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科研費研究者番号 : 50455573
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山本, 雄広
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ヤマモト, タケヒロ
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Romanization |
Yamamoto, Takehiro
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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 : 50383774
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2016
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科学研究費補助金研究成果報告書
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2015
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この研究では, がんの進展に伴うメチル化反応の動態を基質供給, すなわちメチル化反応の唯一の基質であるS-アデノシルメチオニン(SAM)の代謝に注目して解析した。固形腫瘍を形成している生きた動物モデルを用いて含硫代謝物の半定量的質量イメージングによるin vivoメタボロミクス解析を行うことで, エピジェネティック変異の形成にかかわるがんの代謝を時空間的に明らかにした。
In this study, we focused on S-adenosylmethionine (SAM) metabolism. SAM is the only substrate in which is used in all the methylation reaction in vivo. In an experimental model of xenograft transplantation of human colon cancer HCT116 cells in superimmunodeficient NOG mice, snap-frozen liver tissues containing metastatic tumors were examined by quantitative-imaging mass spectrometry. As reported previously, short hairpin CD44 RNA interference (shCD44) in cancer cells caused significant regression of tumor growth in the host liver. Under these circumstances, the CD44 knockdown suppressed polyamines (polyamines are biosynthesized from SAM), GSH and energy charges.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2013~2015
課題番号 : 25513008
研究分野 : メタボロミクス
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