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J. Biol. Chem., Vol. 280, Issue 14, 13641-13647, April 8, 2005

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Lipocalin 2 Diminishes Invasiveness and Metastasis of Ras-transformed Cells^*

Jun-ichi Hanai, Tadanori Mammoto, Pankaj Seth, Kiyoshi Mori¶, S. Ananth Karumanchi, Jonathan Barasch¶, and Vikas P. Sukhatme||

From the Divisions of Nephrology and Hematology-Oncology, Department of Medicine and Center for Study of the Tumor Microenvironment, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215 and ^¶Department of Medicine and Anatomy and Cell Biology, College of Physicians and Surgeons, Columbia University, New York, New York 10032

Lipocalin 2, an iron-siderophore-binding protein, converts embryonic kidney mesenchyme to epithelia. We found that lipocalin 2 could also convert 4T1-Ras-transformed mesenchymal tumor cells to an epithelial phenotype, increase E-cadherin expression, and suppress cell invasiveness in vitro and tumor growth and lung metastases in vivo. The Ras-MAPK pathway mediated the epithelial to mesenchymal transition in part by increasing E-cadherin phosphorylation and degradation. Lipocalin 2 antagonized these effects at a point upstream of Raf activation. Lipocalin 2 action was enhanced by iron-siderophore. These data characterize lipocalin 2 as an epithelial inducer in Ras malignancy and a suppressor of metastasis.

Received for publication, November 18, 2004 , and in revised form, January 25, 2005.

^* 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.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Figs. A–C.

These authors contributed equally to this work.

^|| To whom correspondence should be addressed: 330 Brookline Ave., RW 563, Beth Israel Deaconess Medical Center, Boston, MA 02215. Tel.: 617-667-2105; Fax: 617-667-7843; E-mail: vsukhatm{at}bidmc.harvard.edu.

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