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J. Biol. Chem., Vol. 279, Issue 44, 46326-46334, October 29, 2004

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Brg-1 Is Required for Maximal Transcription of the Human Matrix Metalloproteinase-2 Gene^*

Zhendong Ma, Mi Jung Chang, Reesha Shah, Jill Adamski, Xueyan Zhao, and Etty N. Benveniste

From the Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294-0005

Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases whose aberrant expression are correlated with tumor invasion and angiogenesis. The transcription factors Sp1, Sp3, and AP-2 are required for constitutive expression of MMP-2 in tumor cells; however, the regulatory mechanisms of MMP-2 expression are not well understood. We investigated the involvement of Brg-1, the ATPase subunit of the SWI/SNF complex, in human MMP-2 gene transcription. Reconstitution of Brg-1 enhances MMP-2 transcription in Brg-1-deficient SW-13 cells. Chromatin immunoprecipitation assay demonstrates that Brg-1 is required for recruitment of Sp1, AP-2, and polymerase II to the MMP-2 promoter, whereas the binding of Sp3 to the MMP-2 promoter is decreased upon Brg-1 reconstitution. Furthermore, Sp1 interacts with Brg-1 in vivo. Restriction enzyme accessibility assays indicate that accessibility of the MMP-2 promoter region is not changed in the absence or presence of Brg-1. These results illustrate the connection between the SWI/SNF complex and optimal expression of MMP-2 and highlight the critical function of Brg-1 in regulating the recruitment of Sp1, Sp3, AP-2, and polymerase II to the MMP-2 promoter.

Received for publication, May 17, 2004 , and in revised form, July 23, 2004.

^* This work was supported in part by National Institutes of Health (NIH) Grants CA-97247, NS-39954, and MH-63650 (to E. N. B.). 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.

Supported in part by the Medical Scientist Training Program at the University of Alabama at Birmingham and currently supported by NIH Predoctoral Fellowship T32 AR-07450.

To whom correspondence should be addressed: Dept. of Cell Biology, McCallum Basic Sciences Building 395, University of Alabama at Birmingham, Birmingham, AL 35294-0005. Tel.: 205-934-7667; Fax: 205-975-6748; E-mail: tika{at}uab.edu.

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