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Submitted on December 19, 2001
Accepted on June 11, 2002
IN ZR-75 BREAST CANCER CELLS
1 Department of Veterinary Physiology & Pharmacology; Department of Biochemistry and Biophysics; Department of Veterinary Anatomy and Public Health, Texas A&M University, College Station, TX
* To whom correspondence should be addressed. 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 (HIF1) protein within 3 h after treatment, whereas estrogen receptor (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 E2-induced pS2 gene expression (mRNA levels) and estrogen response element-dependent reporter gene activity in ZR-75 cells. Although E2 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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degradation •
proteasome •
ZR-75 cells •
breast cancer
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