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This version published online on June 26, 2003
Endocrinology, doi:10.1210/en.2003-0294
A more recent version of this article appeared on October 1, 2003
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Submitted on March 5, 2003
Accepted on June 13, 2003

Estrogen and Progesterone Upregulate Glucose Transporter Expression in ZR-75-1 Human Breast Cancer Cells*

Rodolfo A. Medina1*, Ana Maria Meneses1, Juan Carlos Vera1, Catherine Guzman1, Francisco Nualart1, Allisson Astuya1, María de los Angeles García1, Sumie Kato1, Andrés Carvajal1, Mauricio Pinto1, and Gareth I. Owen1

1 Laboratorio de Biología Celular y Molecular, MIFAB, Universidad Nacional Andrés Bello, Republica 217, Piso 4, Santiago, Chile; Departamento de Fisiopatología, Departamento de Histología y Embriología, Departamento de Biología Molecular, Facultad de Ciencias Biológicas, Universidad de Concepción, Barrio Universitario S/N, Concepción, Chile; Departamento de Endocrinología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda 340, Santiago, Chile.

* To whom correspondence should be addressed. E-mail: rmedina{at}unab.cl.

Breast cancer incidence increases in women receiving combined estrogen and progesterone therapy. Breast tumors show increased expression of the glucose transporter GLUT1. We determined the effect of these hormones on GLUT1-4 expression and on deoxyglucose transport in ZR-75-1 breast cancer cells. Immunoblotting, immunocytochemistry, flow cytometry and RT-PCR showed that GLUT1 expression is upregulated by progesterone and, to a greater degree, by combined therapy. GLUT2 expression is unaffected by hormonal treatment. GLUT3 protein and RNA is upregulated by progesterone and combined therapy and GLUT4 protein expression is upregulated by all hormonal treatments. Deoxyglucose transport studies revealed the presence of three transport components with characteristics corresponding to GLUT1/4, GLUT2 and GLUT3. 17{beta}-estradiol produced a slight increase in transport at the Km corresponding to GLUT3. Progesterone produced a small increase in transport at the Km corresponding to GLUT1/4 and combined 17{beta}-estradiol and progesterone produced a small increase in transport at the Km corresponding to GLUT3 and a large increase in transport at the Km corresponding to GLUT1/4. This indicates that 17{beta}-estradiol and progesterone differentially regulate GLUT1-4 expression and that these changes correlate to changes in glucose uptake. We postulate that combined hormone replacement therapy provides a survival advantage to developing ZR-75 breast cancer cells.
Key words: glucose transporters • estrogen • progesterone • breast cancer




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