c-mycとbcl-2プロトオンコゲンの間の協力的な相互作用

A Fanidi¹, E A Harrington, G I Evan

¹Biochemistry of the Cell Nucleus Laboratory, Imperial Cancer Research Fund, London, UK.

Nature

|October 8, 1992

まとめ

BCL-2タンパク質は,MYC腫瘍遺伝子が誘発するアポトーシスを防止し,これらの腫瘍遺伝子ががんの発症と薬剤耐性においてどのように協力するかについての新しいメカニズムを明らかにします.

科学分野:

腫瘍学腫瘍学
分子生物学は分子生物学である.
細胞生物学細胞生物学

背景:

BCL-2プロトオンコゲンはBリンパ球腫瘍で活性化され,腫瘍進行においてMYCオンコゲンと作用する.
アポトーシスを抑制するBCL-2の役割は,その機能の鍵ですが,MYCとの相乗効果は完全に理解されていません.
MYCは細胞分裂 (ミトゲネシス) を促進し,プログラム細胞死 (アポトシス) を誘導することが知られている.

研究の目的:

BCL-2とMYCの腫瘍遺伝子の相乗効果のメカニズムを調査する.
BCL-2タンパク質がMYC誘発のアポトーシスを特定的にブロックできるかどうかを判断する.
この相互作用ががんと薬剤耐性における影響を理解するために.

主な方法:

MYC誘発のアポトーシスに対するBCL-2タンパク質発現の影響を調査した.
BCL-2がMYCのミトジェニック機能に影響するかどうかを評価した.

主要な成果:

BCL-2タンパク質は,MYCによって誘発されたアポプトシスを特に取り消します.
BCL-2はMYCのミトゲン機能に影響を与えない.
この相互作用は,腫瘍遺伝子の協力のための新しいメカニズムを提供します.

結論:

BCL-2とMYCの腫瘍遺伝子は,MYC誘発のアポトーシスを抑制するBCL-2の能力を通じて協力する.
この発見は,がん発生と腫瘍における薬剤耐性の発達を理解するために重要である.
潜在的な治療的影響を持つ腫瘍遺伝子の協力のための新しい経路を特定しました.

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