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FBR-MuSV的fos癌基因转化的未定型小鼠结缔组织细胞的寿命延长和致瘤性

Extended life span and tumorigenicity of nonestablished mouse connective tissue cells transformed by the fos oncogene of FBR-MuSV.

作者信息

Jenuwein T, Müller D, Curran T, Müller R

出版信息

Cell. 1985 Jun;41(2):629-37. doi: 10.1016/s0092-8674(85)80035-0.

Abstract

We have analyzed the transforming potential of two fos oncogene products in nonestablished cultures of mouse connective tissue cells: p55fos of FBJ-MuSV and p75gag-fos of FBR-MuSV. Although both proteins induced morphological transformation and colony formation at low cell density in a G418 resistance selection assay, p75gag-fos exhibited more pronounced transforming potential than p55fos. In addition, p75gag-fos-transformed cells overcame crisis with a high probability and were tumorigenic in syngenic mice. These properties of the FBR-MuSV appear to be linked to structural alterations in the p75gag-fos oncogene product. Polyoma virus large T protein complemented the transforming potential of fos, in that it not only increased the probability of establishment of fos-transformed cells but also enhanced fos-induced morphological transformation. Our results suggest that different oncogenes affect morphological transformation, low cell density growth, establishment, and tumorigenicity to various degrees.

摘要

我们分析了两种Fos癌基因产物在小鼠结缔组织细胞非定型培养物中的转化潜力:FBJ-MuSV的p55Fos和FBR-MuSV的p75gag-Fos。尽管在G418抗性选择试验中,这两种蛋白在低细胞密度下均诱导了形态转化和集落形成,但p75gag-Fos表现出比p55Fos更显著的转化潜力。此外,p75gag-Fos转化的细胞极有可能克服危机,并在同基因小鼠中具有致瘤性。FBR-MuSV的这些特性似乎与p75gag-Fos癌基因产物的结构改变有关。多瘤病毒大T蛋白补充了Fos的转化潜力,因为它不仅增加了Fos转化细胞建立的概率,还增强了Fos诱导的形态转化。我们的结果表明,不同的癌基因对形态转化、低细胞密度生长、建立和致瘤性有不同程度的影响。

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