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Blood, Vol. 94 No. 5 (September 1), 1999:
pp. 1701-1710
Interleukin-9-Induced Expression of M-Ras/R-Ras3 Oncogene in T-Helper
Clones
Jamila Louahed,
Luigi Grasso,
Charles De Smet,
Emiel Van Roost,
Claude Wildmann,
Nicholas C. Nicolaides,
Roy C. Levitt, and
Jean-Christophe Renauld
From the Ludwig Institute for Cancer Research, Brussels Branch, and
the Experimental Medicine Unit, Université Catholique de Louvain,
Brussels, Belgium; and Magainin Institute of Molecular Medicine,
Plymouth Meeting, PA.
In an attempt to gain insight into the molecular mechanisms involved
in interleukin-9 (IL-9) activities, representational difference
analysis (RDA) was used to identify messages that are induced by IL-9
in a murine T-helper-cell clone. One of the isolated genes encodes for
the newly described M-Ras or R-Ras3, which is part of the Ras gene
superfamily. M-Ras expression was found to be induced by IL-9 but not
IL-2 or IL-4 in various murine T-helper-cell clones, and this
induction seems to be dependent on the JAK/STAT pathway. Contrasting
with the potent upregulation of M-Ras expression, M-Ras was not
activated by IL-9 at the level of guanosine triphosphate/guanosine diphosphate (GTP/GDP) binding. However, IL-3 increased GTP
binding to M-Ras, suggesting that M-Ras induction might represent a new mechanism of cooperativity between cytokines such as IL-3 and IL-9.
Constitutively activated M-Ras mutants induced activation of Elk
transcription factor by triggering the MAP kinase pathway and allowed
for IL-3-independent proliferation of BaF3 cells. Taken together,
these results show that cytokines such as IL-9 can regulate the
expression of a member of the RAS family possibly involved in
growth-factor signal transduction.
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