肝がんの治療における脆弱性の誘発と利用
Cun Wang1,2, Serena Vegna3, Haojie Jin1,2
1State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Nature
|October 4, 2019
まとめ
肝臓がん細胞の衰老を誘導する. 抗うつ剤のサートラリンは mTOR信号を遮断することで これらの細胞を選択的に殺し 肝臓がん治療の新たな戦略を提示します
科学分野:
- 腫瘍学
- 分子生物学
- 薬理学について
背景:
- 肝臓がん,特に肝細胞癌は 効果的な治療法が限られている.
- ソラフェニブのような既存の治療法は わずかな効果があります
- 細胞の老化を誘導し,その後,老化を誘導することは,潜在的な治療戦略です.
研究 の 目的:
- 肝臓がんの新たな治療標的を特定する
- 肝臓がん細胞の衰老を誘発するCDC7抑制の役割を調査する.
- 衰えつつある肝臓がん細胞を 選択的に排除する薬を発見するためです
主な方法:
- CDC7を標的として識別する キノムに焦点を当てた遺伝子スクリーンです
- セノリチス剤を検出し セルトラリンを検出する
- CDC7とmTORの信号伝達経路を阻害する.
- 肝臓がんのマウスモデルです
主要な成果:
- CDC7の薬理学的抑制は,TP53変異の肝がん細胞の老化を選択的に誘導する.
- セルトラリンは,CDC7抑制された老化細胞を選択的に殺す老化剤として特定されました.
- CDC7とmTORのシグナル伝達を併せて抑制すると,mTORの抑制とアポトーシスが持続した.
- 併用療法により,マウスモデルでの腫瘍の成長が著しく減少した.
結論:
- セルトラリンのような薬で 衰老を誘発するために CDC7を標的とするのは 肝がんに対する有望な戦略です
- CDC7とmTOR抑制の組み合わせは,有意な抗腫瘍効果を示しています.
- 誘発された脆弱性を利用することで 肝臓がんの治療に 新たなアプローチが生まれます
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