DCCは,依存性受容体活性を通じて腫瘍の進行を抑制する
Marie Castets1, Laura Broutier, Yann Molin
1Apoptosis, Cancer and Development Laboratory - Equipe labellisée La Ligue, LabEx DEVweCAN, Centre de Cancérologie de Lyon, INSERM U1052-CNRS UMR5286, Université de Lyon, Centre Léon Bérard, 69008 Lyon, France.
Nature
|December 14, 2011
まとめ
大腸がん (DCC) で削除されたタンパク質は,がん細胞死亡を誘導することによって腫瘍を抑制します. DCCの損失について
科学分野:
- 腫瘍学 腫瘍学
- 分子生物学は分子生物学である.
- 遺伝学 遺伝学とは
背景:
- 腫瘍抑制剤として結腸直腸がん (DCC) でデリテッドの役割は議論されている.
- DCC遺伝子発現は,進行 kolorektal がんでは減少しています.
- DCCは依存性受容体として作用し,ネットリン-1に結合しない限りアポトーシスを誘発する.
研究 の 目的:
- 腫瘍進行におけるDCC誘発のアポトーシスの役割を調査する.
- DCCの機能喪失が,攻撃的ながんの発症を誘発するかどうかを判断する.
- DCCのプロアポプトティック活動を静止するマウスモデルを作成するために.
主な方法:
- マウスにおけるDCCのプロアポプトシス活性に対する遺伝的沈黙.
- 自発的な腸内腫瘍の観察.
- APCミュータントの文脈における腸内腫瘍数と攻撃性の評価.
主要な成果:
- DCC誘発のアポプトーシスの喪失は,低頻度で自発的な腸内腫瘍症につながる.
- DCC機能喪失は,APC変異マウスの腸内腫瘍数と攻撃性を増加させる.
- 侵襲性の高いアデノカルシノーマの発症が観察されました.
結論:
- DCCは,腫瘍細胞のアポトーシスを誘発することによって,腫瘍抑制剤として機能します.
- DCC誘発のアポトーシスは,腫瘍の進行を制御する上で重要な役割を果たします.
- DCCのアポプトシス機能の喪失は,結腸直腸がんの発症と攻撃性に寄与する.
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