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Cell Growth & Differentiation, Vol 5, Issue 12 1381-1387, Copyright © 1994 by American Association of Cancer Research
ARTICLES |
C Lin, Q Wang, VM Maher and JJ McCormick
Department of Microbiology, Michigan State University, East Lansing 48824.
To determine whether the human c-fes gene, a homologue of the feline v-fes oncogene, can play a role in the malignant transformation of human fibroblasts, we transfected a near-diploid, infinite life span, growth factor-independent, human fibroblast cell strain, MSU-1.2, with plasmids carrying a fes gene along with a selectable marker. The fes gene was either the v-fes oncogene from the Gardner-Arnstein strain of feline sarcoma virus or a chimeric construct in which 835 base pairs representing exons 10-19 from the human c-fes proto-oncogene had been substituted for the corresponding feline sequence in the v-fes oncogene. The transfected cells were selected in appropriate medium, and a number of drug-resistant clones were isolated, and the progeny cells were assayed for fes expression by immunoprecipitation analysis. Six independent clones that expressed the v-fes protein and four that expressed the gag-c-fes protein were further characterized. The former exhibited anchorage independence and formed progressively growing, invasive, spindle cell sarcomas in athymic mice after only a short latency period. The latter strains were not anchorage independent and did not form tumors in athymic mice. These results show that the v-fes oncogene can malignantly transform an infinite life span human fibroblast cell strain, but the human c-fes gene cannot.
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