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ウィルムスの腫瘍抑制剤WT1によるインスリン型の成長因子II遺伝子の抑制
I A Drummond1, S L Madden, P Rohwer-Nutter
1Howard Hughes Medical Institute, University of Chicago, IL 60637.
Science (New York, N.Y.)
|July 31, 1992
まとめ
ウィルムスの腫瘍抑制遺伝子WT1は抑制剤として働き,インスリン類似成長因子II (IGF-II) の転写を制御する. この発見は,ウィルムズ腫瘍におけるIGF-II過剰発現と,腎臓発育におけるWT1の役割を説明する.
科学分野:
- 分子生物学は分子生物学である.
- 発達生物学 発達生物学について
- 癌の遺伝学 癌の遺伝学
背景:
- ウィルムズ腫瘍は小児性腎臓がんであり,しばしば胎児のミトゲンであるインスリン類似成長因子II (IGF-II) の過剰発現と関連している.
- ウィルムズ腫瘍抑制剤遺伝子 (WT1) は,典型的には抑制剤として作用する転写因子をコードする.
研究 の 目的:
- WT1がIGF-II転写を調節する分子メカニズムを調査する.
- WT1が直接IGF-IIプロモーターを抑制し,ウィルムスの腫瘍の病原性におけるその役割を決定する.
主な方法:
- トランジエンント・トランスフェクション・アッセイは,胎児の主要なIGF-IIプロモーター領域を定義するために使用されました.
- IGF-IIプロモーターへのWT1結合は,in vivoで評価されました.
- レポーター遺伝子アッセイは,IGF-II転写に対するWT1の抑制活動を測定するために使用されました.
主要な成果:
- 胎児における主要なIGF-IIプロモーターは,ニュクレオチド -295から+135.5までの領域にマッピングされました.
- WT1は,このプロモーター領域内の複数のサイトに結合することが判明しました.
- WT1は,体内でIGF-II転写の強力な抑制を示し,最大抑制は,転写開始部位に隣接するWT1結合部位に依存した.
結論:
- WT1は,胎児の主要なIGF-IIプロモーターを直接抑制し,ウィルムズ腫瘍におけるIGF-II過剰発現の分子説明を提供する.
- WT1は,腎臓の発達中にIGF-IIの産生を制限することによって,ブラスタム細胞の増殖を否定的に調節する.
- これらの発見は,腎臓の発達とウィルムスの腫瘍発生における重要な規制軸を強調しています.
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