Premium
Modulation by the src oncogene of the effect of inhibitory diffusible factor IDF45
Author(s) -
Blat C.,
Villaudy J.,
Rouillard D.,
Golde A.,
Harel L.
Publication year - 1987
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041300315
Subject(s) - inhibitory postsynaptic potential , modulation (music) , proto oncogene tyrosine protein kinase src , microbiology and biotechnology , oncogene , biology , chemistry , genetics , cell , neuroscience , physics , phosphorylation , cell cycle , acoustics
Density‐dependent inhibition of growth has been assumed to be under the control of inhibitory molecules diffusing from dense cell cultures. Growth inhibitory factors have been fractionated or purified from medium conditioned by different cell types. In the present work, it was shown that IDF45 (inhibitory factor diffusing from 3T3 cells) decreased DNA synthesis in chick embryo fibroblats (CEF) and was an inhibitor of CEF growth; this inhibition was reversible. Since similitudes between oncogene products and growth factors have been observed, it was of interest to compare the inhibitory effect of IDF45 upon the stimulation of DNA synthesis induced either by serum or by pp60‐src. CEF infected by Ny68 virus (a mutant of Rous sarcoma virus ts for the expression of transformation) were density‐inhibited at 41°C, but were stimulated at this temperature by addition of 1% serum. This stimulation was 94% inhibited by IDF45. The same Ny68‐infected cells could also be stimulated transfer to 37°C, the permissive temperature (in the absence of serum). The stimulation of DNA synthesis by src expression was poorly inhibited by IDF45. From our results, it appears that oncogene expression in CEF induces a loss in their sensitivity to IDF45. This would explain why transformed cells escape DDI of growth.