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Vol. 12, Issue 6, 1859-1868, June 2001
and
*Department of Molecular Pathogenesis and We investigated the production of hyaluronan (HA) and its effect on
cell motility in cells expressing the v-src mutants.
Transformation of 3Y1 by v-src virtually activated HA
secretion, whereas G2A v-src, a nonmyristoylated form of
v-src defective in cell transformation, had no effect.
In cells expressing the temperature-sensitive mutant of v-Src, HA
secretion was temperature dependent. In addition, HA as small as 1 nM,
on the other side, activated cell motility in a tumor-specific manner.
HA treatment strongly activated the motility of v-Src-transformed 3Y1,
whereas it showed no effect on 3Y1- and 3Y1-expressing G2A
v-src. HA-dependent cell locomotion was strongly blocked
by either expression of dominant-negative Ras or treatment with a Ras
farnesyltransferase inhibitor. Similarly, both the MEK1 inhibitor and
the kinase inhibitor clearly inhibited HA-dependent cell locomotion. In
contrast, cells transformed with an active MEK1 did not respond to the
HA. Finally, an anti-CD44-neutralizing antibody could block the
activation of cell motility by HA as well as the HA-dependent
phosphorylation of mitogen-activated protein kinase and Akt. Taken
together, these results suggest that simultaneous activation of the
Ras-mitogen-activated protein kinase pathway and the phosphoinositide
3-kinase pathway by the HA-CD44 interaction is required for the
activation of HA-dependent cell locomotion in v-Src-transformed cells.
Department
of Orthopaedic Surgery, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan; and The
Institute for Molecular Science of Medicine, Aichi Medical University,
Yazako, Nagakute, Aichi 480-1195, Japan
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