D. Poisson Paré¹, D. Song^1,2, V. Luu-The¹, B. Han^1,2, S. Li^1,2, G. Liu², F Labrie¹ and G. Pelletier<sup>1

1</sup>Molecular Endocrinology and Oncology Research Center, Laval University Hospital Research Center, 2705 Laurier blvd, Quebec City, Qc, Canada, G1V 4G2. ²First Hospital of Jilin University, Changchun, China.

Abstract

It is known that the steroid sulfatase (STS) and the estrogen sulfotransferase (EST1E1) are commonly expressed in human breast carcinomas. STS and EST1E1 combined action could maintain the equilibrium between sulfated (inactive) and unconjugated (active) estrogens, which might have effects on development of hormone dependent breast cancer. We studied the expression of the STS and EST1E1 in 88 breast carcinomas and 57 adjacent non-malignant tissues by immunohistochemistry. The results were correlated with the tumor expression of estrogen receptor α (ER-α) and β (ER-β), progesterone receptor A (PR-A) and B (PR-B) and the proliferation marker CDC47, the tumoral type and stage and the age at surgery. STS expression was higher in carcinoma specimens than in adjacent normal tissues, although not to a significant level (p = 0.064) and it was positively associated with CDC47 expression (p  0.05). These observations support the hypothesis that STS is overexpressed in breast cancer and associated with a worse prognosis. EST1E1 was observed for the first time in the nuclei of epithelial and tumoral cells. Tumor expression of EST1E1 was positively correlated with ER-β (p  0.01) and PR-B (p  0.05), two steroid receptors already associated with an improve prognosis for breast cancer. Controlling the STS overexpression in carcinomas could be a way to inhibit cancer growth. The significance of the association between EST1E1 and ER-β or PR-B should be further studied since these two receptors are transcription activators and may regulate the expression of protective enzymes like EST1E1.