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KAKEN_16K08349seika.pdf
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Download
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:179.4 KB
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| Last updated |
:Oct 31, 2019 |
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Total downloads since Oct 31, 2019 : 335
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| Title |
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胃発がんリスク亢進に繋がるピロリ菌感染宿主細胞の分子特性解析
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| Kana |
イ ハツガン リスク コウシン ニ ツナガル ピロリキン カンセン シュクシュ サイボウ ノ ブンシ トクセイ カイセキ
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I hatsugan risuku kōshin ni tsunagaru pirorikin kansen shukushu saibō no bunshi tokusei kaiseki
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Molecular characterization of H. pylori-infected cells associated with the development of gastric cancer
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津川, 仁
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ツガワ, ヒトシ
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Tsugawa, Hitoshi
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慶應義塾大学・医学部 (信濃町) ・講師
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Research team head
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科研費研究者番号 : 30468483
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2019
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科学研究費補助金研究成果報告書
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2018
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H. pylori感染胃粘膜において、酸化ストレス依存的に発生するCAPZA1過剰発現細胞は、オートファジー発現不全細胞であり、H. pylori感染を受ける事で癌蛋白質CagA蓄積を介してCD44v9発現癌幹細胞へと進展することが明らかとなった。これらの結果から、CAPZA1発現とその機能制御論の構築により、H. pylori感染胃粘膜における癌幹細胞発生予防論の開発に繋がると期待される。
Helicobacter pylori-derived CagA plays a role as an oncogenic driver in gastric epithelial cells. However, upon delivery into gastric epithelial cells, CagA is usually degraded by autophagy. We report that enhancement of lysosome associated membrane protein 1 (LAMP1) expression is necessary for autophagolysosome formation. In contrast, CAPZA1 inhibits the LAMP1 expression in the nuclei. Thus, in CAPZA1-overexpressing gastric epithelial cells infected with H. pylori, autophagolysosome formation is inhibited and CagA escapes autophagic degradation. These findings identify CAPZA1 as a novel negative regulator of autophaglysosome formation and suggest that deregulation of CAPZA1 expression leads to increased risk of gastric carcinogenesis. Our findings demonstrate that regulation of autophagy by CAPZA1 could be a central mechanisms to account for the effects of CagA on gastric carcinogenesis, and represent new insight for understanding and manipulating the development of gastric cancer.
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研究種目 : 基盤研究 (C) (一般)
研究期間 : 2016～2018
課題番号 : 16K08349
研究分野 : 分子細菌学
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