激活的N-ras控制了HT1080人类纤维瘤细胞的转变表型
H Paterson1, B Reeves, R Brown
1Institute of Cancer Research, Chester Beatty Laboratories, London, U.K.
Cell
|December 4, 1987
概括
在HT1080纤维瘤细胞中激活的N-ras瘤基因驱动了转变的表型. 复原细胞显示N-ras p21水平降低,表明它在维持癌细胞特征方面起着至关重要的作用.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 该N-ras瘤基因与各种癌症有关.
- 人类纤维瘤细胞具有激活的N-ras瘤基因.
- 了解瘤基因功能对于癌症治疗至关重要.
研究的目的:
- 为了确定HT1080细胞中激活的N-ras瘤基因是否有助于它们的转变表型.
- 研究N-ras在维持癌细胞特征中的作用.
主要方法:
- 从HT1080纤维肉瘤细胞中分离平面复原细胞系.
- 对染色体 ploidy 和 N-ras 基因的复制数进行分析.
- 免疫沉以量化N-ras p21基因产物水平.
- 通过转染与克隆的ras瘤基因进行反转化检测.
主要成果:
- 回归系表现出增加的染色体性,但没有增加N-ras转换等位基因拷贝.
- 与HT1080.0相比,在复原细胞中证实了较低的突变N-ras p21水平.
- 来自复原细胞的瘤显示转化等位基剂量增加.
- 通过引入激活的ras瘤基因,可以通过引入激活的ras瘤基因重新转化复原细胞.
结论:
- 激活的N-ras瘤基因直接参与维持HT1080人类纤维瘤细胞的转变表型.
- 对于这种细胞系的恶性特征来说,N-ras瘤基因的剂量和表达是至关重要的.
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