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高いc-myc発現は,ヒトリンパ腫細胞におけるSV40DNAの複製を促進する
M Classon1, M Henriksson, J Sümegi
1Department of Tumor Biology, Karolinska Institute, Stockholm, Sweden.
Nature
|November 19, 1987
まとめ
c-myc遺伝子産物の過剰発現は,ヒトリンパ腫細胞におけるシミアンウイルス40 (SV40) の複製を促進する. これは,c-mycがDNA複製プロセスを制御する上で重要な役割を果たしていることを示唆しています.
科学分野:
- 分子生物学は分子生物学である.
- 腫瘍学 腫瘍学
- ウイルス学 ウイルス学 ウイルス学
背景:
- v-myc腫瘍遺伝子は,様々な組織にわたって腫瘍を誘発する.
- c-mycプロトオンコゲンは,活性化によって様々な腫瘍の発達に関与しています.
- c-myc遺伝子製品は,細胞増殖とDNA合成を調節する核フォスフォタンパク質です.
研究 の 目的:
- シミアンウイルス40 (SV40) の複製におけるc-mycの役割を調査する.
- c-mycの過剰発現が,通常は劣っている細胞でSV40の複製を回復できるかどうかを判断する.
主な方法:
- SV40ベースのベクトル (pSVEpR4) レプリケーションアッセイを活用した.
- BJABリンパ腫細胞の複製を,バーキットリンパ腫線と比較した.
- c-myc発現コンストラクタによるBJAB細胞の共同感染を行った.
主要な成果:
- SV40ベクターはBJAB細胞では不十分複製されたが,高c-myc発現のBurkittリンパ腫系では効率的に複製された.
- c-mycコンストクトによる共感染は,BJAB細胞におけるSV40複製を10倍に増加させた.
- c-myc過剰発現がヒトリンパ腫細胞におけるSV40複製を促進することを実証した.
結論:
- c-myc遺伝子製品は,DNA複製を制御する上で重要な役割を果たします.
- c-mycの過剰発現は,特定のヒト細胞系におけるSV40複製の制限を克服することができます.
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