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Autocrine growth induced by kinase type oncogenes in myeloid cells requires AP‐1 and NF‐M, a myeloid specific, C/EBP‐like factor.
Author(s) -
Sterneck E.,
Müller C.,
Katz S.,
Leutz A.
Publication year - 1992
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.1460-2075.1992.tb05034.x
Subject(s) - biology , autocrine signalling , myeloid , cancer research , nfkb1 , myeloid cells , kinase , growth factor , microbiology and biotechnology , cell culture , biochemistry , transcription factor , gene , genetics , receptor
The nuclear oncogenes v‐myc or v‐myb specifically transform avian myeloid cells. In both cases, the transformed cells remain dependent on chicken myelomonocytic growth factor (cMGF). This factor dependence can be relieved by expression of kinase‐type oncogenes such as v‐mil or v‐erbB, leading to expression of cMGF and autocrine growth stimulation. In erythroid cells the same kinase‐type oncogenes cause transformation but do not induce cMGF expression. Here we investigated the molecular mechanisms of the observed lineage specific oncogene collaboration. We found that kinase‐type oncogenes and TPA activate the cMGF promoter via AP‐1 like transcription factors. The activation of the cMGF promoter is, however, strictly dependent on the binding of nuclear proteins to both halves of an inverted repeat adjacent to the AP‐1 binding site. These proteins are related to C/EBP. They are expressed exclusively in myeloid cells and were therefore termed NF‐M. Our results indicate that the lineage specific cooperation of kinase type oncogenes with v‐myb or v‐myc in leukemia formation is based on the concerted action of AP‐1 and NF‐M on the cMGF promoter.