基因rrg的表达与由LTR-c-H-ras转换的NIH 3T3的逆转相关
S Contente1, K Kenyon, D Rimoldi
1Department of Pathology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799.
概括
通常存在于NIH 3T3细胞中的老鼠基因rrg在癌症发育过程中被抑制. 恢复转化细胞中的RRG表达逆转了瘤形成,表明其作为瘤抑制剂的作用.
科学领域:
- 分子生物学分子生物学
- 癌症研究 癌症研究
- 细胞转化细胞的转化.
背景情况:
- 基因rrg通常表达在小鼠NIH 3T3细胞中.
- 由LTR-c-H-ras诱导的细胞转化降低了RRG表达的调节.
- 干扰素治疗可能导致持续的复原细胞系与重新表达的RRG.
研究的目的:
- 研究RRG基因在细胞转化和瘤发生中的作用.
- 确定rrg的再表达是否可以逆转转变的表型并抑制瘤形成.
主要方法:
- 对 rrg 基因进行部分补充DNA的分离.
- 持久性复原细胞的稳定转化与反感和感觉表达矢量.
- 在裸体小鼠中评估细胞形态,RRG信使RNA水平和瘤性.
主要成果:
- 反感RRG表达载体诱导了转变的表型,减少了RRGmRNA,并导致逆转细胞中的瘤性.
- 感官表达载体没有影响复原细胞的正常表型,信息水平或非瘤起源性.
- 转化细胞中RRG的再表达与瘤发生性丧失相关.
结论:
- 这种RRG基因作为瘤抑制剂起作用.
- 对rrg的下调对转化和瘤原性表型的发展至关重要.
- 调节RRG表达为癌症提供了潜在的治疗策略.
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