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Differential Effects of Estrogen on cAMP Production in MCF7 Cells
Author(s) -
Chan Robbie,
Lee KamLen Daniel,
Chan Albert
Publication year - 2006
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.20.4.a542-c
Subject(s) - forskolin , estrogen , endocrinology , estrogen receptor , medicine , chemistry , receptor , intracellular , estrogen receptor beta , hormone , biology , biochemistry , cancer , breast cancer
The classical view of the molecular actions of estrogen is described by its interaction with the intracellular estrogen receptor (ER), the binding of hormone‐receptor complex to the estrogen response element (ERE) on the DNA and followed by the alterations of gene expressions. Recently it has been reported that membrane estrogen receptor (mER) exist and it is suggested to be G protein linked receptor. In this report we show that under steroid‐free culture conditions supplemented with low percentage of charcoal‐stripped serum, differential estrogen treatments of human breast cancer MCF7 cells induce different responses of cAMP productions. Labeling MCF7 cells with [2‐ 3 H]adenine for 16 hours and treating the same MCF7 cells with nanomolar scale of estrogen for 30 minutes did not change the ratio of [ 3 H]cAMP : total [ 3 H]adenine nucleotides (ATP+ADP+cAMP), as determined by column chromatography, when compared with the control. Estrogen, however, significantly enhanced forskolin‐stimulated cAMP production when compared with the ratio of cAMP/Total measured in cells stimulated with forskolin alone (> 1.5‐fold). On the contrary, pre‐treating MCF7 cells with the same concentration of estrogen for 24 hours before the assay, the hormone significantly decreased the basal cAMP level and cAMP production stimulated with forskolin when compared with their corresponding values under acute estrogen treatment. Our data suggest that estrogen exerts differential effects on the cAMP production in MCF7 cells, possibly involving the activations G α i and G α s family of G proteins, depending on the length of time of hormone treatment.