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オートファギーは,循環するアルギニンによって腫瘍の成長を維持する
Laura Poillet-Perez1, Xiaoqi Xie1, Le Zhan1
1Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.
Nature
|November 16, 2018
まとめ
ホストのオートファギーは アルギニンのレベルを維持することで 癌をサポートします 宿主体における自殺を阻害すると 肝臓アルギナーゼIが放出され アルギニンが枯渇し 腫瘍は飢えることになります アルギニンの回復は 部分的に腫瘍の成長を救います
科学分野:
- 細胞生物学
- メタボリズム
- 癌 生物学
背景:
- オートファギーは細胞の代謝と生存に不可欠であり,特に栄養素欠乏期には重要です.
- がん細胞は成長と生存のためにオートファギーを利用しますが,腫瘍の進行における宿主のオートファギーの役割は複雑です.
- マウスの自己死性の遺伝子の全身的消去は代謝と腫瘍の成長に影響し,宿主自己死性の役割を示唆する.
研究 の 目的:
- 宿主オートファギーの腫瘍増殖への影響を研究する.
- ホストのオートファジーが腫瘍の進行に影響を与える代謝メカニズムを特定する.
- ガンにおける宿主自閉症を標的とした治療戦略を探求する.
主な方法:
- 成人マウスの主体特異的な自己死遺伝子の削除 (Atg7,Atg5)
- 腫瘍アロ移植と腫瘍の成長の評価
- 血清タンパク質解析とアルギニンの体内代謝追跡
- アルギニンの栄養補充
主要な成果:
- 宿主特異的なAtg7の消去は,複数のアロ移植腫瘍の成長を阻害しました.
- ホストのオートファギーの喪失は,循環中のアルギニンのレベルを低下させ,循環中のアルギナーゼI (ARG1) を増加させた.
- 肝臓特有のAtg7の消去はこれらの効果を模倣し,アルギニンの補給は部分的に腫瘍の成長を回復させた.
結論:
- 欠陥のある宿主自閉症により 肝臓はARG1を放出し 腫瘍の成長に不可欠な循環アルギニンを分解します
- これはがんにおける代謝の脆弱性を特定し,宿主オートファギーはアルギニンの供給を維持することによって腫瘍の進行をサポートします.
- ホストのオートファジーやアルギニンの代謝をターゲットにすることで,がん治療の潜在的治療法となる.
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