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[Cancer Research 59, 4225-4227, September 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 4225-4227, September 1, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Correlation between Expression of the Matrix Metalloproteinase-1 Gene in Ovarian Cancers and an Insertion/Deletion Polymorphism in Its Promoter Region1

Yasunobu Kanamori, Mieko Matsushima, Takeo Minaguchi, Kanji Kobayashi, Satoru Sagae, Ryuichi Kudo, Naoki Terakawa and Yusuke Nakamura2

Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639 [Y. K., M. M., T. M., Y. N.]; Department of Obstetrics and Gynecology, Tottori University School of Medicine, Yonago [Y. K., N. T.]; and Department of Obstetrics and Gynecology, Sapporo Medical University School of Medicine, Hokkaido [K. K., S. S., R. K.], Japan

Matrix metalloproteinases (MMPs), a family of closely related enzymes that degrade the extracellular matrix, are likely to be involved in invasion and metastasis of tumor cells. A guanine (G) insertion/deletion polymorphism within the promoter region of MMP-1 influences the transcription of this gene; i.e., the 2G (insertion-type) promoter possesses greater transcriptional activity than the 1G (deletion-type) promoter. To investigate whether this feature contributes to cancer development and/or progression, we genotyped 163 ovarian cancer patients for the polymorphism and then analyzed levels of expression of the MMP-1 gene in their tumors. The proportion of patients who were either heterozygotes or homozygotes for the 2G allele was significantly higher than that observed among 150 individuals without cancer (P = 0.028). Moreover, the levels of MMP-1 expression in cancer tissues among the patients carrying 2G alleles were elevated significantly in comparison with 1G homozygotes (P = 0.0038). By stimulating degradation of extracellular matrix, an excess of MMP-1 production may enhance development and/or rapid progression of ovarian cancers.




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Copyright © 1999 by the American Association for Cancer Research.