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Endocrinology Vol. 143, No. 2 467-475
Copyright © 2002 by The Endocrine Society

RECEPTORS

Activation of Antimetastatic Nm23-H1 Gene Expression by Estrogen and Its {alpha}-Receptor

Kwang-Huei Lin, Won-Jing Wang, Yi-Hsin Wu and Sheue-Yann Cheng

Department of Biochemistry (K.-H.L., W.-J.W., Y.-H.W.), Chang-Gung University, Taoyuan, Taiwan, Republic of China; and Gene Regulation Section (S.-y.C.), Laboratory of Molecular Biology, Combined Cancer Research Center, National Cancer Institute, Bethesda, Maryland 20892

Address all correspondence and requests for reprints to: K. H. Lin, Chang-Gung University, Taoyuan, Taiwan, Republic of China. E-mail: khlin{at}mail2000.com.tw

Metastasis of various malignant cells is inversely related to the abundance of the Nm23-H1 protein. The role of estrogens in tumor metastasis has now been investigated by examining the effect of E2 on the expression of the Nm23-H1 gene. Three human breast carcinoma cell lines, in which endogenous ER{alpha} is expressed at different levels, were used as a tool to assess the role of ER{alpha} in Nm23-H1 gene-mediated metastasis. E2 induced time-dependent increases in the abundance of Nm23-H1 mRNA and protein, with the extent of these effects correlating with the level of expression of ER{alpha}. E2 induced a marked decrease in the invasive activity of MCF-7 and BT-474 cells but had no effect on BCM-1 cells, which had virtually no ER{alpha}. Consistent with these results, the ER-mediated Nm23-H1 promoter activity was inhibited 3-fold by the E2 antagonist, ICI 182,780. Deletion analysis of the promoter region of the Nm23-H1 gene identified a positive estrogen-responsive element located in -108/-94. ER protein bound specifically to the -108/-79 fragment with high avidity. These results indicate that E2, acting through ER{alpha}, activated transcription of the Nm23-H1 gene via a positive estrogen-responsive element in the promoter region of the gene. These results suggest that E2 could suppress tumor metastasis by activating the expression of the Nm23-H1 gene.




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