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J. Biol. Chem., Vol. 279, Issue 17, 17634-17639, April 23, 2004
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From the
Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan, the ¶Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060-8638, Japan, the ||Pharmaceutical Research Laboratory, Kirin Brewery Company Ltd., 3 Miyahara, Takasaki, Gunma 370-1295, Japan, the **Division of Molecular Pharmacology, Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Toshima-ku, Tokyo 170-8455, Japan, and the Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037
Autotaxin (ATX) is a tumor cell motility-stimulating factor originally isolated from melanoma cell supernatant that has been implicated in regulation of invasive and metastatic properties of cancer cells. Recently, we showed that ATX is identical to lysophospholipase D, which converts lysophosphatidylcholine to a potent bioactive phospholipid mediator, lysophosphatidic acid (LPA), raising the possibility that autocrine or paracrine production of LPA by ATX contributes to tumor cell motility. Here we demonstrate that LPA and ATX mediate cell motility-stimulating activity through the LPA receptor, LPA1. In fibroblasts isolated from lpa1-/- mice, but not from wild-type or lpa2-/-, cell motility stimulated with LPA and ATX was completely absent. In the lpa1-/- cells, LPA-stimulated lamellipodia formation was markedly diminished with a concomitant decrease in Rac1 activation. LPA stimulated the motility of multiple human cancer cell lines expressing LPA1, and the motility was attenuated by an LPA1-selective antagonist, Ki16425. The present study suggests that ATX and LPA1 represent potential targets for cancer therapy.
Received for publication, December 19, 2003 , and in revised form, January 20, 2004.
* This work was supported in part by research grants from the Ministry of Education, Culture, Sports, Science, and Technology and the Human Frontier Special Program. The costs of publication of this article were defrayed in part by the payment of page charges. This 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. Tel.: 81-3-5842-4723; Fax: 81-3-3818-3173; E-mail: jaoki{at}mol.f.u-tokyo.ac.jp.
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