支配的なマイナスのMYCは,ABL腫瘍遺伝子の変換を阻害する

C L Sawyers¹, W Callahan, O N Witte

¹Department of Medicine, Howard Hughes Medical Institute, University of California, Los Angeles 90024.

Cell

|September 18, 1992

まとめ

MYCの高いレベルはABLの腫瘍遺伝子と相乗効果がある. 支配的マイナスのMYCはABL誘発変異を抑制し,c-MYCを証明した.

科学分野:

オンコゲノミクスとは
細胞の変容細胞の変容
分子生物学は分子生物学である.

背景:

MYC腫瘍遺伝子の発現は,しばしばABL腫瘍遺伝子と連携する.
ABL媒介による変換におけるMYCの正確な役割については,さらなる解明が必要である.

研究の目的:

MYCがABLの腫瘍遺伝子主導の細胞変異に不可欠であるかどうかを調査する.
MYCがABLの腫瘍遺伝子の変換を補完するか,欠かせないかどうかを判断する.

主な方法:

繊維芽細胞における支配的陰性MYCタンパク質の過剰発現.
支配的陰性MYCがv-ablおよびBCR-ABL腫瘍遺伝子によって誘発される変異に与える影響を評価する.
主要マウス骨髄のpre-B細胞の変容を評価し,BCR-ABLとMYCを共発するレトロウイルス構造を用いた.

主要な成果:

支配的なマイナスのMYCはv-ablとBCR-ABL腫瘍遺伝子の変換を5〜10倍に減少させた.
セリン/スレオニンキナーゼオンコゲンv-mosによって誘発された変換は影響を受けませんでした.
主導的マイナスのMYCは,マウスの骨髄前B細胞の最初のBCR-ABL媒介変換を抑制しました.

結論:

c-MYCは,ABLの腫瘍遺伝子の媒介による細胞変異に不可欠です.
これらの発見は,MYCとABLが腫瘍形成に関与する分子経路を定義するのに役立ちます.

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