Abstract:
Simian sarcoma virus-transformed NIH 3T3 (SSV-NIH 3T3) and SSV-NRK cells secrete a potent growth-promoting activity identical with the platelet-derived growth factor (PDGF) in mitogenic assays. The secreted activity is blocked by anti-PDGF antisera and competes with 125I-PDGF for receptor binding, suggesting that the secreted protein is the transforming protein of SSV, p28v-sis, or its processed product. Secreted p28v-sis appears to stimulate autocrine cell growth of SSV-transformed cells because anti-PDGF antisera block 3H-thymidine incorporation into growing SSV-NIH 3T3 and SSV-NRK cells. SSV-transformed cells have reduced numbers of high-affinity 125I-PDGF receptors; PDGF/p28v-sis receptor was purified from SSV-NIH 3T3 cells and retained active protein tyrosine kinase activity stimulated by PDGF. The rate of tumor growth in athymic nude mice injected with SSV-transformed cells was compared with levels of secreted growth factor activity. The rate of tumor growth in nude mice correlated directly with levels of p28v-sis secreted by SSV-transformed cells.
Keywords: Animal Cell Division Cell Line *Cell Transformation, Neoplastic Cells, Cultured Kidney Kinetics Mice Mice, Inbred Strains Peptides/*PHYSIOLOGY Platelet-Derived Growth Factor/METABOLISM Protein Kinases/GENETICS Rats Receptors, Cell Surface/*PHYSIOLOGY Retroviridae/*GENETICS Sarcoma Viruses, Simian/*GENETICS Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. Viral Proteins/GENETICS JOURNAL ARTICLE
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