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J. Biol. Chem., Vol. 277, Issue 33, 30271-30282, August 16, 2002
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From the Department of Biological Sciences, Korea Advanced
Institute of Science and Technology, Taejon 305-701, South Korea
A rate-limiting step of tumor cell metastasis is
matrix degradation by active matrix metalloproteinases (MMPs). It is
known that reactive oxygen species are involved in tumor metastasis. Sustained production of H2O2 by phenazine
methosulfate (PMS) induced activation of pro-MMP-2 through the
induction of membrane type 1-MMP (MT1-MMP) expression in HT1080 cells.
MMP-2, MMP-9, and tissue inhibitor of metalloproteinase-1 and -2 levels
were changed negligibly by PMS. A one time treatment with
H2O2 did not induce activation of MMPs. It was
also demonstrated that superoxide anions and hydroxyl radicals were not
related to PMS action. PMS-induced pro-MMP-2 activation was regulated
by the receptor tyrosine kinases, especially the receptors of
platelet-derived growth factor and vascular endothelial growth factor,
and downstream on the phosphatidylinositol 3-kinase/NF-
Sustained Production of H2O2
Activates Pro-matrix Metalloproteinase-2 through Receptor Tyrosine
Kinases/Phosphatidylinositol 3-Kinase/NF-
B Pathway*
B pathway but
not Ras, cAMP-dependent protein kinase, protein kinase C,
and mitogen-activated protein kinases. PMS did not induce pro-MMP-2
activation in T98G and NIH3T3 cells. This may be related to a low level
of MT1-MMP, indicating a threshold level of MT1-MMP is important for
pro-MMP-2 activation. Furthermore, PMS increased cell motility and
invasion but decreased cell-cell interaction. Cell-matrix interaction
was not affected by PMS.
*
This work was supported by a grant of the Korea Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea
(02-PJ1-PG10-20801-0001).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Biological
Sciences, Korea Advanced Institute of Science and Technology, Taejon
305-701, South Korea. Tel.: 82-42-869-2625; Fax: 82-42-869-2610; E-mail: aschung@mail.kaist.ac.kr.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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