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PMID: 1906157 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Suppression of c-myc and c-myb is tightly linked to terminal differentiation induced by IL6 or LIF and not growth inhibition in myeloid leukemia cells.

Oncogene ·Vol. 6 ·No. 6 ·1991-06-00 ·Pages 903-9

Hoffman-Liebermann B, Liebermann DA

Abstract

Cell proliferation and differentiation are intimately related processes where the proto-oncogenes c-myc and c-myb have been implicated to play a role. Previously, we have shown that both c-myc and c-myb were induced in normal myeloid precursors when the cells were stimulated for growth, were expressed in the autonomously proliferating myeloid leukemic M1 cell line and were rapidly suppressed in both normal and M1 cells following induction of terminal differentiation associated with growth arrest. In order to distinguish molecular events associated with terminal differentiation versus those due to growth inhibition, as well as to increase our understanding of the role of the proto-oncogenes c-myc and c-myb in both of these cellular processes, in this work we have studied the expression of c-myc and c-myb in M1 cells induced for growth inhibition associated with terminal differentiation (via treatment with the physiological inducers IL6 or leukemia inhibitory factor mean value of LIF), partial differentiation (using IL1 or LPS) or no detectable differentiation properties (using IFN beta or IFN gamma). We show that, for all the treatments used in this study, down regulation of the proto-oncogenes c-myc and c-myb occurred only when M1 cells were stimulated to undergo terminal differentiation. In addition, we transfected the M1 cell line with a vector containing the c-myc gene under control of the beta-actin promoter, so that c-myc was no longer down regulated by IL6 or LIF. Previously, we have shown that in the presence of the myeloid differentiation inducers IL6 or LIF, these M1myc cells were blocked at an intermediate stage of myeloid differentiation and continued to proliferate. In sharp contrast to their altered response to IL6 or LIF, M1myc cells were as responsive as the parental M1 cells to growth suppression by the different antiproliferative compounds which do not induce terminal differentiation. Thus, continued expression of c-myc had no effect on growth suppression induced by IL1, IFN beta, IFN gamma and LPS. Taken together, these results indicate that c-myc and c-myb down regulation is not necessary for growth suppression, but down regulation of c-myc is, and c-myb may be, essential for terminal differentiation.

MeSH Terms
Animals Blotting, Northern Cell Differentiation/drug effects,physiology Cell Division/drug effects,physiology Down-Regulation/drug effects Gene Expression Regulation, Leukemic/drug effects,physiology Growth Inhibitors Interferon Type I/pharmacology Interferon-gamma/pharmacology Interleukin-1/pharmacology Interleukin-6/pharmacology Leukemia Inhibitory Factor Leukemia, Myeloid/metabolism,pathology,physiopathology Lipopolysaccharides/pharmacology Lymphokines/pharmacology Mice Proto-Oncogene Proteins/genetics,metabolism Proto-Oncogene Proteins c-myb Proto-Oncogene Proteins c-myc/genetics,metabolism Suppression, Genetic/genetics,physiology
Chemicals
Growth Inhibitors Interferon Type I Interleukin-1 Interleukin-6 Leukemia Inhibitory Factor Lif protein, mouse Lipopolysaccharides Lymphokines Proto-Oncogene Proteins Proto-Oncogene Proteins c-myb Proto-Oncogene Proteins c-myc Interferon-gamma
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Hoffman-Liebermann B
Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia 19104.
Liebermann D A
Article Info
Journal
Oncogene
Abbr.
Oncogene
ISSN
0950-9232
Published
1991-06-00
Pages
903-9
Language
English
Region
England
NLM ID
8711562
Subset
IM
Grants
NCI NIH HHS · 1R01CA43618-01 · United States
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