アクティベーションされたN-rasは,ヒト線維肉腫細胞HT1080の変異したフェノタイプを制御します
H Paterson1, B Reeves, R Brown
1Institute of Cancer Research, Chester Beatty Laboratories, London, U.K.
Cell
|December 4, 1987
まとめ
HT1080繊維肉腫細胞の活性化されたN-ras腫瘍遺伝子は,変異したフェノタイプを駆動する. リバータント細胞は,N-ras p21レベルが低下したことを示し,がん細胞の特徴を維持する上で重要な役割を果たしていることを示しました.
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:
- N-ras腫瘍遺伝子は,様々ながんに関与しています.
- HT1080ヒト線維肉腫細胞は,活性化されたN-ras腫瘍遺伝子を有する.
- 腫瘍遺伝子の機能を理解することは,がん治療において極めて重要です.
研究 の 目的:
- HT1080細胞の活性化されたN-rasオンコゲンが,それらの変異したフェノタイプに寄与するかどうかを判断する.
- 癌細胞の特徴を維持するN-rasの役割を調査する.
主な方法:
- HT1080繊維肉腫細胞からフラットリバータント細胞系を分離.
- 染色体プロイディとN-rasアレル複製数の分析.
- N-ras p21遺伝子産物レベルを定量化するための免疫プレシピテーション.
- 再変異は,クローン化されたRASオンコゲンとのトランスフェクションによる検査である.
主要な成果:
- リバータント系は染色体プロイディの増加を示したが,N-ras変異アレル複製の増加は認められなかった.
- 変異したN-ras p21の低いレベルは,HT1080.0と比較してリバータント細胞で確認されました.
- リバータント細胞から派生した腫瘍は,変異性アレル投与量の増加を示した.
- リバータント細胞は,活性化されたRAS腫瘍遺伝子を導入することで再変形させることができる.
結論:
- 活性化されたN-ras腫瘍遺伝子は,ヒト線維肉腫細胞HT1080の変異したフェノタイプの維持に直接参加する.
- N-ras腫瘍遺伝子の投与量と発現は,この細胞系における悪性特性を決定的に有する.
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