Analysis of the 17β-estradiol (17BE2)-dependent ESR1, CARM1, NCOA3 and POLR2A cistromes in human H3396 breast cancer cells

2019 ◽  
Author(s):  
DG Ceschin
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
17Β Estradiol

17β-estradiol (E2) induces cdc25A gene expression in breast cancer cells by genomic and non-genomic pathways

2006 ◽  
Vol 99 (1) ◽  
pp. 209-220 ◽  
Author(s):  
Wan Ru Lee ◽  
Chien-Cheng Chen ◽  
Shengxi Liu ◽  
Stephen Safe
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
17Β Estradiol

Ceramide synthases CerS4 and CerS5 are upregulated by 17β-estradiol and GPER1 via AP-1 in human breast cancer cells

2014 ◽  
Vol 92 (4) ◽  
pp. 577-589 ◽  
Author(s):  
Marthe-Susanna Wegner ◽  
Ruth Anna Wanger ◽  
Stephanie Oertel ◽  
Sebastian Brachtendorf ◽  
Daniela Hartmann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
17Β Estradiol ◽  
Ceramide Synthases

NDV‐D90 inhibits 17β‐estradiol‐mediated resistance to apoptosis by differentially modulating classic and nonclassic estrogen receptors in breast cancer cells

2020 ◽  
Vol 122 (1) ◽  
pp. 3-15
Author(s):  
Peng Shan ◽  
Bo Tang ◽  
Shanshan Xie ◽  
Zengling Zhang ◽  
Jiehou Fan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptors ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
17Β Estradiol

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 ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Glucose Transporter ◽  
Combined Therapy ◽  
Hormone Replacement ◽  
Breast Cancer Incidence ◽  
Hormonal Treatment ◽  
Glut1 Expression ◽  
17Β Estradiol

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.

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