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Originally published In Press as doi:10.1074/jbc.M008681200 on November 1, 2000

J. Biol. Chem., Vol. 276, Issue 2, 1164-1172, January 12, 2001
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KiSS-1 Represses 92-kDa Type IV Collagenase Expression by Down-regulating NF-kappa B Binding to the Promoter as a Consequence of Ikappa Balpha -induced Block of p65/p50 Nuclear Translocation*

Chunhong Yan, Heng Wang, and Douglas D. BoydDagger

From the Department of Cancer Biology, MD Anderson Cancer Center, Houston, Texas 77030

The 92-kDa type IV collagenase (MMP-9) plays a critical role in tissue remodeling. We undertook a study to determine whether the KiSS-1 gene, previously shown to suppress cancer spread (metastases), negatively regulates MMP-9 expression. Six cell lines positive for MMP-9 mRNA were deficient in KiSS-1 mRNA. One of these cell lines, HT-1080, stably transfected with a KiSS-1 expression construct, demonstrated substantially lower MMP-9 enzyme activity/protein and in vitro invasiveness. The lower MMP-9 enzyme activity reflected reduced steady-state mRNA levels which, in turn, was due to attenuated transcription. Activation of ERKs and JNKs by phorbol 12-myristate 13-acetate and tumor necrosis factor alpha , respectively, leading to increased MMP-9 amounts was not antagonized by KiSS-1 expression, suggesting that MAPK pathways modulating MMP-9 synthesis are not the target of KiSS-1. Although MMP-9 expression is regulated by AP-1, Sp1, and Ets transcription factors, KiSS-1 did not alter the binding of these factors to the MMP-9 promoter. However, NF-kappa B binding to the MMP-9 promoter required for expression of this collagenase was reduced by KiSS-1 expression. Diminished NF-kappa B binding reflected less p50/p65 in the nucleus secondary to increased Ikappa Balpha levels in the cytosols of the KiSS-1 transfectants. Thus, KiSS-1 diminishes MMP-9 expression by effecting reduced NF-kappa B binding to the promoter.

* This work was supported by National Institutes of Health Grants R01 CA58311, R01 DE10845, and P50 DE11906-01 (to D. B.).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.

Dagger To whom correspondence should addressed: Dept. of Cancer Biology, Box 179, MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030. Tel.: 713-792-8953; Fax: 713-745-1927; E-mail: dboyd@mdanderson.org.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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