Effects of estrogen on leptin gene promoter activation in MCF-7 breast cancer and JEG-3 choriocarcinoma cells: selective regulation via estrogen receptors α and β

Leptin is a potential regulator of conceptus development. We have previously suggested that in primate pregnancy, leptin biosynthesis is regulated by estrogen in a tissue-specific manner. Therefore, the objective of the current study was to determine the mechanism of estrogen action on LEP promoter...

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Bibliographic Details
Published in:Molecular and cellular endocrinology 2001-05, Vol.176 (1), p.67-75
Main Authors: O'Neil, Jennifer S, Burow, Matthew E, Green, Amy E, McLachlan, John A, Henson, Michael C
Format: Article
Language:English
Subjects:
Antiestrogens
Breast Neoplasms - metabolism
Choriocarcinoma - metabolism
Estradiol - analogs & derivatives
Estradiol - pharmacology
Estrogen
Estrogen Antagonists - pharmacology
Estrogen Receptor alpha
Estrogen Receptor beta
Female
Fulvestrant
Genes, Reporter - genetics
Humans
JEG-3 (choriocarcinoma cells)
Leptin
Leptin - genetics
MCF-7 (breast cancer cells)
Promoter Regions, Genetic - genetics
Receptors, Estrogen - genetics
Receptors, Estrogen - metabolism
Response Elements - genetics
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - genetics
RNA, Messenger - metabolism
Transcriptional Activation - drug effects
Transfection
Tumor Cells, Cultured
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Summary:Leptin is a potential regulator of conceptus development. We have previously suggested that in primate pregnancy, leptin biosynthesis is regulated by estrogen in a tissue-specific manner. Therefore, the objective of the current study was to determine the mechanism of estrogen action on LEP promoter activation in divergent cell types. The effects of estrogen were investigated in estrogen receptor (ER)-positive MCF-7 breast cancer cells and in ER-negative JEG-3 choriocarcinoma cells. Cells were transfected with a leptin-luciferase or an estrogen responsive element (ERE)-luciferase reporter construct, in conjunction with ERα, ERβ, or empty vector expression plasmids. Cells were treated with estradiol and/or the specific estrogen antagonists, ICI-182,780 or 4-hydroxytamoxifen. In MCF-7 cells, estradiol stimulated ( P
ISSN:0303-7207
1872-8057
DOI:10.1016/S0303-7207(01)00473-7