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Amplified expression of three jun family members inhibits erythroleukemia
differentiation
EV Prochownik, MJ Smith, K Snyder and D Emeagwali
Department of Pediatrics, University of Michigan School of Medicine, Ann
Arbor.
Several different proto-oncogenes have been shown to influence cellular
differentiation. One of the most widely studied model systems has been the
Friend murine erythroleukemia cell (F-MELC) line, which can be induced to
undergo erythroid differentiation by a variety of chemical agents.
Constitutive overexpression of either the c-myc or c-myb proto- oncogenes
has been previously shown to inhibit F-MELC differentiation, whereas c-myc
antisense sequences accelerate the process. To investigate the potential
involvement of other proto-oncogenes and immediate early response genes in
F-MELC differentiation, we studied the expression of the three known
members of the jun family as well as another gene, egr-1, which, like the
jun family members, is expressed as an immediate early response gene in
growth factor-stimulated quiescent cells. All four genes were expressed in
F-MELC, although the levels of expression and modes of regulation differed.
Transfection with amplifiable c-jun, junB, or junD expression plasmids
inhibited differentiation, whereas transfection with an egr-1 expression
plasmid was without effect. These results indicate that jun family members
play a role in mediating F-MELC differentiation. The known inhibitory
effect of phorbol ester tumor promoters on F-MELC differentiation may be
the result of their known stimulation of jun expression.
Volume 76,
Issue 9,
pp. 1830-1837,
11/01/1990
Copyright © 1990 by The American Society of Hematology
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