scholarly journals Estrogen and Progesterone Up-Regulate Glucose Transporter Expression in ZR-75-1 Human Breast Cancer Cells

Endocrinology ◽  
2003 ◽  
Vol 144 (10) ◽  
pp. 4527-4535 ◽  
Author(s):  
Rodolfo A. Medina ◽  
Ana Maria Meneses ◽  
Juan Carlos Vera ◽  
Catherine Guzman ◽  
Francisco Nualart ◽  
...  

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 deoxyglucose transport in ZR-75-1 breast cancer cells. Immunoblotting, immunocytochemistry, flow cytometry, and RT-PCR showed that GLUT1 expression is up-regulated by progesterone and, to a greater degree, combined therapy. GLUT2 expression is unaffected by hormonal treatment. GLUT3 protein and RNA is up-regulated by progesterone and combined therapy, and GLUT4 protein expression is up-regulated by all hormonal treatments. Deoxyglucose transport studies revealed the presence of three transport components with characteristics corresponding to GLUT1/4, GLUT2, and GLUT3. 17β-Estradiol produced a slight increase in transport at the Michaelis constant (Km) corresponding to GLUT3. Progesterone produced a small increase in transport at the Km corresponding to GLUT1/4, and combined 17β-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 17β-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.

Surgery Today ◽  
2008 ◽  
Vol 38 (10) ◽  
pp. 911-920 ◽  
Author(s):  
Yoshiaki Kanaya ◽  
Hiroyoshi Doihara ◽  
Kouji Shiroma ◽  
Yutaka Ogasawara ◽  
Hiroshi Date

2006 ◽  
Vol 99 (1) ◽  
pp. 209-220 ◽  
Author(s):  
Wan Ru Lee ◽  
Chien-Cheng Chen ◽  
Shengxi Liu ◽  
Stephen Safe

Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1621
Author(s):  
Azadeh Nilchian ◽  
Nikolina Giotopoulou ◽  
Wenwen Sun ◽  
Jonas Fuxe

Transforming growth factor beta 1 (TGF-β1) is associated with epithelial-mesenchymal transition (EMT), lymph metastasis, and poor prognosis in breast cancer. Paradoxically, TGF-β1 is also a potent inhibitor of cell proliferation. TGF-β1-induced EMT involves activation of several pathways including AKT, which also regulates glucose uptake. Recent data show that prolonged TGF-β1 exposure leads to a more stable EMT phenotype in breast cancer cells. However, whether this is linked to changes in glucose metabolism is not clear. Here, we used a model of TGF-β1-induced EMT in mammary epithelial cells to study the regulation of Glut1 and EMT markers during the induction compared to a prolonged phase of EMT by western blot, immunofluorescence and qPCR analysis. We also measured cell proliferation and uptake of the glucose analogue 2-NDBG. We found that EMT induction was associated with decreased Glut1 expression and glucose uptake. These effects were linked to reduced cell proliferation rather than EMT. Knockdown of Glut1 resulted in growth inhibition and less induction of vimentin during TGF-β1-induced EMT. Intriguingly, Glut1 levels, glucose uptake and cell proliferation were restored during prolonged EMT. The results link Glut1 repression to the anti-proliferative response of TGF-β1 and indicate that re-expression of Glut1 during chronic TGF-β1 exposure allows breast cancer cells to develop stable EMT and proliferate, in parallel.


2014 ◽  
Vol 92 (4) ◽  
pp. 577-589 ◽  
Author(s):  
Marthe-Susanna Wegner ◽  
Ruth Anna Wanger ◽  
Stephanie Oertel ◽  
Sebastian Brachtendorf ◽  
Daniela Hartmann ◽  
...  

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