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and ß in human lung adenocarcinoma cells
1 Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY 40292, USA
2 Department of Biology, Bellarmine University, Louisville, KY 40205, USA
3 Department of Pharmacology and Toxicology, Center for Genetics and Molecular Medicine, University of Louisville School of Medicine, Louisville, KY 40292, USA
(Requests for offprints should be addressed to C M Klinge; Email: carolyn.klinge{at}louisville.edu)
The higher frequency of lung adenocarcinoma in women smokers than in men smokers suggests a role for gender-dependent factors in the etiology of lung cancer. We evaluated estrogen receptor (ER)
and ß expression and activity in human lung adenocarcinoma cell lines and normal lung fibroblasts. Full-length ER and ERß proteins were expressed in all cell lines with higher ERß than ER. Although estradiol (E2) binding was similar, E2 stimulated proliferation only in cells from females, and this response was inhibited by anti-estrogens 4-hydroxytamoxifen (4-OHT) and ICI 182,780. In contrast, E2 did not stimulate replication of lung adenocarcinoma cells from males and 4-OHT or ICI did not block cell proliferation. Similarly, transcription of an estrogen response element-driven reporter gene was stimulated by E2 in lung adenocarcinoma cells from females, but not males. Progesterone receptor (PR) expression was increased by E2 in two out of five adenocarcinoma cell lines from females, but none from males. E2 decreased E-cadherin protein expression in some of the cell lines from females, as it did in MCF-7 breast cancer cells, but not in the cell lines from males. Thus, ER and ERß expression does not correlate with the effect of ER ligands on cellular activities in lung adenocarcinoma cells. On the other hand, coactivator DRIP205 expression was higher in lung adenocarcinoma cells from females versus males and higher in adenocarcinoma cells than in normal human bronchial epithelial cells. DRIP205 and other ER coregulators may contribute to differences in estrogen responsiveness between lung adenocarcinoma cells in females and males.
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