[Functional interaction between estrogen receptor and proto-oncogene products c-Jun and c-Fos].
We show here that TPA treatment of MCF-7 cells represses estrogen receptor dependent transcriptional activity, while increasing the AP1 binding activity. These two events are probably linked, since the transcriptional activity of the estrogen receptor in these cells is repressed by overexpression of both cJun or cFos, the components of the AP1 transcripts factor. On the contrary no repression was observed after overexpression of another member of the jun family, the JunD. The repression caused by cJun or cFos may depend on partially different pathways. Our results suggest that the inhibition of TPA of the estrogen dependent growth of the MCF-7 cells is caused by over expression of cJun and cFos.
Doucas
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UA 1149 du CNRS, Département des Biotechnologies, Institut Pasteur, Paris.
Yaniv
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M
D004347:Drug Interactions / Q000235:genetics; D004794:Enzyme Repression / Q000235:genetics; D008908:Mink Cell Focus-Inducing Viruses / Q000187:drug effects / Q000235:genetics; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics*; D016755:Proto-Oncogene Proteins c-jun / Q000235:genetics*; D011960:Receptors, Estrogen / Q000235:genetics*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014158:Transcription, Genetic / Q000187:drug effects
D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D011960:Receptors, Estrogen; D013755:Tetradecanoylphorbol Acetate
Interaction fonctionnelle entre le récepteur d'oestrogène et les produits des proto-oncogènes c-Jun et c-Fos.