活性化されたKi-rasで破壊されたヒト大腸がん細胞系の変化した成長

S Shirasawa¹, M Furuse, N Yokoyama

¹Department of Genetics, Kyushu University, Fukuoka, Japan.

Science (New York, N.Y.)

|April 2, 1993

まとめ

Ki-ras遺伝子の変異を活性化すると,細胞の成長と分化が変化し,結腸直腸がんを誘発する. がん細胞におけるこれらの突然変異を妨害することで,腫瘍の成長とc-myc発現が減少しました.

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:

Ki-rasプロトオンコゲンを活性化する点変異は,ヒトの結腸直腸腫瘍の約50%で発見されています.
結腸直腸腫瘍形成における活性化Ki-rasの特定の役割は,さらなる機能的調査を必要とします.

研究の目的:

結腸直腸がんにおけるKi-ras変異の活性化の機能的意義を調査する.
細胞の分化と成長に対する活性化されたKi-rasの影響を明らかにする.

主な方法:

DLD-1とHCT 116の結腸がん細胞系における活性化されたKi-ras遺伝子を破壊するために同類の再結合を使用した.
遺伝子破壊細胞の特徴と,その親細胞の特徴を,形態学,成長,遺伝子発現などと比較した.

主要な成果:

活性化されたキラスの遺伝子が破壊された細胞は,形態学的変化を示した.
固定部独立の成長の減少と減速した増殖率は,in vitroおよびin vivo (裸のマウス) で観察されました.
c-myc腫瘍遺伝子の発現の低下は,活性化されたKi-ras.が欠けている細胞で観察されました.

結論:

活性化されたKi-ras遺伝子は,大腸直腸腫瘍形成において重要な役割を果たします.
活性化されたKi-rasは,細胞の分化と成長経路を調節することにより,結腸直腸がんの発症に影響を与えます.

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