Integration of a mutant c-Ha-ras oncogene into C3H/10T1/2 cells and its relationship to tumorigenic transformation.
Integration of a mutant c-Ha-ras oncogene into C3H/10T1/2 cells and its relationship to tumorigenic transformation.
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突变 c-Ha-ras 癌基因整合到 C3H/10T1/2 细胞中及其与致瘤转化的关系。
DOI:
10.1093/carcin/6.9.1295
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发表时间:
1985
期刊:
影响因子:
4.7
通讯作者:
Fahl,WE
中科院分区:
文献类型:
--
作者:
Manoharan,TH;Burgess,JA;Ho,D;Newell,CL;Fahl,WE
C3H/10T1/2-CL8 mouse cells were shown to take up and express a plasmid-cloned drug resistance gene (Ecogpt) after DNA transfection at a frequency (2−6 × 10−4) which is acceptable for routine recovery of gene-transformed populations. Transfection of 10T1/2 cells with a mutant c-Ha-rasoncogene (pEJ6.6 plasmid) results in neoplastically transformed 10T1/2 cell populations as judged by colony morphology and tumorigenic growth in nude mice. The levels of mutant c-Ha-rasgene integration and expression in the tumorigenic cell populations and 10T1/2 cell controls were determined, and the highest level of mutantrastranscript was seen in the most tumorigenic cell population. A preliminary comparison of 10T1/2 and NIH/3T3 cells showed similar frequencies for pEJ6.6-induced transformed foci and a similar lack of sensitivity to the transforming effects of a cloned B-lymoncogene. The results identify a genetic event, which has previously been shown to be carcinogen-inducible, that is permissive for neoplastic transformation of the widely used carcinogen-transformable 10T1/2 mouse cell line.