scholarly journals Estrogen-induced Proliferation of Uterine Epithelial Cells Is Independent of Estrogen Receptor α Binding to Classical Estrogen Response Elements

2006 ◽  
Vol 281 (36) ◽  
pp. 26683-26692 ◽  
Author(s):  
Jeanne E. O'Brien ◽  
Theresa J. Peterson ◽  
Ming Han Tong ◽  
Eun-Jig Lee ◽  
Liza E. Pfaff ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Epithelial Cells ◽  
Estrogen Receptor Α ◽  
Uterine Epithelial Cells ◽  
Response Elements ◽  
Estrogen Response ◽  
Estrogen Response Elements

scholarly journals The Effect of Relaxin on Cell Proliferation in Mouse Cervix Requires Estrogen Receptor α Binding to Estrogen Response Elements in Stromal Cells

Endocrinology ◽  
2010 ◽  
Vol 151 (6) ◽  
pp. 2811-2818 ◽  
Author(s):  
LiJuan Yao ◽  
Paul S. Cooke ◽  
Daryl D. Meling ◽  
Roger D. Shanks ◽  
J. Larry Jameson ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Stromal Cells ◽  
Estrogen Receptor Α ◽  
Response Elements ◽  
Estrogen Response ◽  
Estrogen Response Elements

scholarly journals Sequence Requirements for Estrogen Receptor Binding to Estrogen Response Elements

1998 ◽  
Vol 273 (45) ◽  
pp. 29321-29330 ◽  
Author(s):  
Mark D. Driscoll ◽  
G. Sathya ◽  
Mesut Muyan ◽  
Carolyn M. Klinge ◽  
Russell Hilf ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Receptor Binding ◽  
Response Elements ◽  
Estrogen Receptor Binding ◽  
Estrogen Response ◽  
Estrogen Response Elements ◽  
Sequence Requirements

scholarly journals Estrogen receptor-α directly regulates the hypoxia-inducible factor 1 pathway associated with antiestrogen response in breast cancer

2015 ◽  
Vol 112 (49) ◽  
pp. 15172-15177 ◽  
Author(s):  
Jun Yang ◽  
Alaa AlTahan ◽  
Dylan T. Jones ◽  
Francesca M. Buffa ◽  
Esther Bridges ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Endocrine Therapy ◽  
Breast Cancer Cells ◽  
Hypoxia Inducible Factor ◽  
Estrogen Receptor Α ◽  
Endocrine Treatment ◽  
Response Elements ◽  
Estrogen Response

A majority of breast cancers are driven by estrogen via estrogen receptor-α (ERα). Our previous studies indicate that hypoxia-inducible factor 1α (HIF-1α) cooperates with ERα in breast cancer cells. However, whether ERα is implicated in the direct regulation of HIF-1α and the role of HIF-1α in endocrine therapy response are unknown. In this study we found that a subpopulation of HIF-1α targets, many of them bearing both hypoxia response elements and estrogen response elements, are regulated by ERα in normoxia and hypoxia. Interestingly, the HIF-1α gene itself also bears an estrogen response element, and its expression is directly regulated by ERα. Clinical data revealed that expression of the HIF-1α gene or a hypoxia metagene signature is associated with a poor outcome to endocrine treatment in ERα+ breast cancer. HIF-1α was able to confer endocrine therapy resistance to ERα+ breast cancer cells. Our findings define, for the first time to our knowledge, a direct regulatory pathway between ERα and HIF-1α, which might modulate hormone response in treatment.

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