Autocrine growth induced by kinase type oncogenes in myeloid cells requires AP-1 and NF-M, a myeloid specific, C/EBP-like factor

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Item Type:	Article
Title:	Autocrine growth induced by kinase type oncogenes in myeloid cells requires AP-1 and NF-M, a myeloid specific, C/EBP-like factor
Creators Name:	Sterneck, E., Mueller, C., Katz, S. and Leutz, A.
Abstract:	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.
Keywords:	AP-1, C/EBP, Growth Factor, Myeloid Transcription Factor, Oncogene Collaboration, Animals, Chickens
Source:	EMBO Journal
ISSN:	0261-4189
Publisher:	Oxford University Press
Volume:	11
Number:	1
Page Range:	115-126
Date:	January 1992
Official Publication:	http://www.ncbi.nlm.nih.gov/pmc/articles/PMC556432/pdf/emboj00086-0122.pdf
PubMed:	View item in PubMed

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