Differentiation of human fibroblasts to tissue macrophages by the Snyder-Theilen feline sarcoma virus is accompanied by nuclear accumulation of the tumor suppressor p53
- F Borellini
- R Glazer
- L Kopelovich
Affiliations: GEORGETOWN UNIV,MED CTR,DEPT PHARMACOL,WASHINGTON,DC 20007. VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. DEPT VET AFFAIRS,LAB CANC GENET & CANC PREVENT,BAY PINES,FL. UNIV S FLORIDA,COLL MED,DEPT PATHOL & CELLULAR & MOLEC BIOL,TAMPA,FL.
- Published online on: March 1, 1996 https://doi.org/10.3892/ijo.8.3.609
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Snyder-Theilen feline sarcoma virus (ST:FeSV)-transduced human fibroblasts differentiate into tissue macrophages with many of the properties of normal macrophages. These cells express high levels of the gag-fes tyrosine kinase fusion protein, p85(v-fes), and exhibit an elevated level of tyrosine phosphorylation. Expression of the macrophage phenotype is accompanied by increased levels of DNA-binding activity and nuclear accumulation of wild-type p53. The DNA-binding activity of the transcription factors Egr-1, CREB and Sp1, which are known to be involved in cell differentiation, is also increased in ST:FeSV-induced macrophages. These observations suggest that v-fes can activate signal transduction pathways normally involved in macrophage differentiation, and that transcription factors such as p53, further facilitate v-fes-induced terminal differentiation.