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c‐Myc‐induced apoptosis in fibroblasts is inhibited by specific cytokines.
Author(s) -
Harrington E.A.,
Bennett M.R.,
Fanidi A.,
Evan G.I.
Publication year - 1994
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1994.tb06630.x
Subject(s) - cancer cell , nucleus , biology , library science , biochemistry , cancer , microbiology and biotechnology , genetics , computer science
We have investigated the mechanism by which deregulated expression of c‐Myc induces death by apoptosis in serum‐deprived fibroblasts. We demonstrate that Myc‐induced apoptosis in low serum is inhibited by a restricted group of cytokines, principally the insulin‐like growth factors and PDGF. Cytokine‐mediated protection from apoptosis is not linked to the cytokines’ abilities to promote growth. Protection from apoptosis is evident in the post‐commitment (mitogen‐independent) S/G2/M phases of the cell cycle and also in cells that are profoundly blocked in cell cycle progression by drugs. Moreover, IGF‐I inhibition of apoptosis occurs in the absence of protein synthesis, and so does not require immediate early gene expression. We conclude that c‐Myc‐induced apoptosis does not result from a conflict of growth signals but appears to be a normal physiological aspect of c‐Myc function whose execution is regulated by the availability of survival factors. We discuss the possible implications of these findings for models of mammalian cell growth in vivo.