title: Apoptotic action of estrogen.
abstract: Estrogen as a mitogen stimulates cell proliferation and prevents cell death in many cell types. In patients, estrogen is known to stimulate breast and uterus cancer development. Ironically, high doses of estrogen can induce regression of hormone-dependent breast cancer in postmenopausal women. The comprehensive mechanism by which estrogen induces tumor recession in breast cancer is still unknown, but activation of the Fas/FasL pathways plays a key role in this process. Laboratory studies show that the apoptotic action of estrogen is the major factor leading to cell number decreases in several cell types. The effects of estrogen are estrogen-receptor dependent. In this mini review, we will focus on the latest findings regarding estrogen apoptotic effects in several cell models, including breast cancer cells, and summarize the possible mechanisms involved in these estrogen mediated processes. New potential implications for the pharmacological control of breast cancer with estrogen in post-menopausal women are also discussed.
authors.affiliation: Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville, VA 22901, USA. rs5wf@virginia.edu
authors.forename: R X-D
authors.initials: RX
authors.lastname: Song
authors.forename: R J
authors.initials: RJ
authors.lastname: Santen
mesh_terms: D017209:Apoptosis; D001943:Breast Neoplasms / Q000378:metabolism; D002455:Cell Division; D004967:Estrogens / Q000378:metabolism / Q000494:pharmacology*; D053222:Fas Ligand Protein; D005260:Female; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism; D008954:Models, Biological; D017698:Postmenopause; D019014:fas Receptor / Q000378:metabolism
chemical_list: D004967:Estrogens; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor