CDC25 フォスファタゼは,潜在的なヒト腫瘍遺伝子の可能性がある
K Galaktionov1, A K Lee, J Eckstein
1Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, NY 11724, USA.
Science (New York, N.Y.)
|September 15, 1995
まとめ
CDC25フォスファタゼは,サイクリン依存キナーゼ (CDK) を活性化する. ヒトの乳がんにおけるCDC25B過剰発現は,CDC25フォスファタゼがヒトの癌発症に寄与することを示唆しています.
科学分野:
- 分子生物学は分子生物学である.
- 細胞生物学 細胞生物学
- 腫瘍学 腫瘍学
背景:
- サイクリン依存キナーゼ (CDK) は細胞サイクルを調節する.
- CDC25フォスファタゼは,阻害性フォスファートを除去することによってCDKを活性化します.
- 人間のCDC25遺伝子ファミリーには,CDC25A,CDC25B,CDC25Cが含まれています.
研究 の 目的:
- 腫瘍性変異におけるCDC25フォスファタゼの役割を調査する.
- CDC25フォスファタゼがヒトの癌発症に寄与するかどうかを判断する.
主な方法:
- ヒトのCDC25A,CDC25B,またはCDC25Cを使用して,ネズミの細胞における腫瘍性焦点形成を評価する.
- 腫瘍性Ha-RASG12VまたはRB1の損失を導入する.
- マウスの腫瘍の特徴を分析する.
- ヒト乳がんサンプルにおけるCDC25B発現を定量化する.
主要な成果:
- 人間のCDC25AとCDC25Bは,CDC25Cではないが,Ha-RASG12VまたはRB1の損失と連携して,歯類の細胞に腫瘍性焦点を形成した.
- 変形した細胞はアヌプロイド性,軟アガー成長を示し,裸のマウスで高級腫瘍を形成した.
- CDC25Bは,ヒトの原発性乳がんの32%で過剰発現していた.
結論:
- CDC25AとCDC25Bのフォスファタゼは,腫瘍性変異を促すことができる.
- 乳がんにおけるCDC25B過剰発現は,ヒトの腫瘍発生における役割を示唆している.
- CDC25フォスファタゼは,ヒトの癌発症に潜在的に寄与する物質である.
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