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Studies on the role of cytosolic sulfotranpsferase SULT1E1 in estrogen signaling in human CA‐HPV‐10 cells
Author(s) -
Kapoor Ruchita,
Sheng Jonathan
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.921.13
Subject(s) - estrogen receptor , estrogen , signal transduction , estrogen receptor beta , transfection , biology , endocrinology , reporter gene , medicine , chemistry , cell culture , microbiology and biotechnology , cancer research , gene expression , cancer , gene , biochemistry , genetics , breast cancer
Human cytosolic sulfotransferase SULT1E1 catalyzes the sulfation of estrogens and estrogenic drugs in human hepatic and non‐hepatic tissues. This estrogen‐preferring sulfotransferase isoform could play a regulatory role in intracellular estrogen signaling activities. Previous studies have suggested that estrogens induce the expression of TFRC, a cell membrane transferrin receptor gene. Studies using DNA microarray and quantitative real‐time PCR methods by our group also showed that TFRC expression was down‐regulated by SULT1E1 transfection in human prostate cancer CA‐HPV‐10 cell line. Because human CA‐HPV‐10 cell line is an estrogen receptor positive cell line, the estrogen receptor‐coupled signaling pathways could relate to the molecular mechanism underlying the observed effect of SULT1E1 on TFRC expression. To test this hypothesis, the effect of SULT1E1 transfection on the estrogen receptor‐coupled signaling pathways was examined using an estrogen response element reporter gene assay in the present studies. The results showed that β‐estradiol was able to induce the estrogen response element controlled reporter gene expression in CA‐HPV‐10 cells. This β‐estradiol‐induced signal transduction process was repressed after the cells were transfected with SULT1E1. These results suggest that SULT1E1 may function as an estrogen signaling mediator in human prostate cancer CA‐HPV‐10 cells.