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[Cancer Research 61, 6755-6761, September 15, 2001]
© 2001 American Association for Cancer Research

Endocrinology

Transcriptional Regulation of the Estrogen-inducible pS2 Breast Cancer Marker Gene by the ERR Family of Orphan Nuclear Receptors1

Desheng Lu, Yoshimitsu Kiriyama, Karen Y. Lee and Vincent Giguère2

Molecular Oncology Group, McGill University Health Centre, Montréal, Québec, H3A 1A1 Canada [D. L., K. Y. L., Y. K., V. G.] and Department of Biochemistry, Medicine and Oncology, McGill University, Montréal, Québec, H3G 1Y6 Canada [V. G.]

The estrogen-receptor-related receptors (ERRs) {alpha}, ß, and {gamma} are orphan nuclear hormone receptors that share significant homology with the estrogen receptors (ERs) but are not activated by natural estrogens. In contrast, the ERRs display constitutive transcriptional activity in the absence of exogenously added ligand. However, the ERRs bind to the estrogen response element and to the extended half-sites of which a subset can also be recognized by ER{alpha}, suggesting that ERRs and ERs may control overlapping regulatory pathways. To test this hypothesis, we explored the possibility that ERRs could regulate the expression of the estrogen-inducible pS2 gene, a human breast cancer prognostic marker. Transfection studies show that all of the ERR isoforms can activate the pS2 promoter in a variety of cell types, including breast cancer cell lines. Surprisingly, sequence analysis combined with mutational studies revealed that, in addition to the well-characterized estrogen response element, the presence of a functional extended half-site within the pS2 promoter is also required for complete response to both ER and ERR pathways. We show that ERR transcriptional activity on the pS2 promoter is considerably enhanced in the presence of all three members of the steroid receptor coactivator family but is completely abolished on treatment with the synthetic estrogen diethylstilbestrol, a recently described inhibitor of ERR function. Finally, we demonstrate that ERR{alpha} is the major isoform expressed in human breast cancer cell lines and that diethylstilbestrol can inhibit the growth of both ER-positive and -negative cell lines. Taken together, these results demonstrate that estrogen-inducible genes such as pS2 can be ERR targets and suggest that pharmacological modulation of ERR{alpha} activity may have therapeutic value in the treatment of breast cancer.




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