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in ZR-75 Breast Cancer Cells
Department of Veterinary Physiology and Pharmacology (M.S., M.W., S.S.), Department of Biochemistry and Biophysics (B.S.), and Department of Veterinary Anatomy and Public Health (D.D., R.B.), Texas A&M University, College Station, Texas 77843-4466
Address all correspondence and requests for reprints to: Stephen Safe, Department of Veterinary Physiology and Pharmacology, Texas A&M University, 4466 TAMU, College Station, Texas 77843-4466. E-mail: ssafe{at}cvm.tamu.edu.
Regulation of estrogen receptor 
(ER) plays an important role in hormone responsiveness and growth of ER-positive breast cancer cells and tumors. ZR-75 breast cancer cells were grown under conditions of normoxia (21% O2) or hypoxia (1% O2 or cobaltous chloride), and hypoxia significantly increased hypoxia-inducible factor 1 protein within 3 h after treatment, whereas ER protein levels were dramatically decreased within 6–12 h, and this response was blocked by the proteasome inhibitor MG-132. In contrast, hypoxia induced only minimal decreases in cellular Sp1 protein and did not affect ER mRNA; however, hypoxic conditions decreased basal and 17ß-estradiol-induced pS2 gene expression (mRNA levels) and estrogen response element-dependent reporter gene activity in ZR-75 cells. Although 17ß-estradiol and hypoxia induce proteasome-dependent degradation of ER, their effects on transactivation are different, and this may have implications for clinical treatment of mammary tumors.
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