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J Biol Chem, Vol. 273, Issue 9, 5248-5252, February 27, 1998
From the The MEN gene (also called
ELL) encodes an RNA polymerase II elongation factor that
has been implicated in t(11;19)(q23;p13.1) translocation in myeloid
leukemias. The function of another elongation factor, elongin, is known
to be inhibited by VHL tumor suppressor protein in vitro,
suggesting the possible relationship of aberrant transcriptional
elongation to oncogenesis. We overexpressed the MEN protein in Rat1
fibroblasts to evaluate its transforming activity. MEN-overexpressing
cells acquired the capacity for anchorage-independent growth. In
addition, the growth factor requirement was decreased in these cells.
However, cells expressing a deletion mutant of MEN lacking the
lysine-rich region did not exhibit such biological abilities. c-Fos
protein expression and AP-1 activity were elevated in the
MEN-expressing cells, which might be part of the mechanism responsible
for the transformation. The c-fos mRNA, the expression of which is known to be regulated partly at the stage of
transcriptional elongation, appeared earlier in the MEN-expressing
cells than in cells transfected with an empty vector or the deletion
mutant lacking the lysine-rich region after stimulation with epidermal growth factor. The RNA polymerase II elongation factor MEN may play an
important role in the regulation of cell proliferation.
Overexpression of the MEN/ELL Protein, an RNA Polymerase II
Elongation Factor, Results in Transformation of Rat1 Cells with
Dependence on the Lysine-rich Region
§,§, and§
Department of Cell Therapy and
Transplantation Medicine and the § Third Department of
Internal Medicine, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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