Estrogen Receptor Synthesis and Turnover in MCF-7 Breast Cancer Cells Measured by a Density Shift Technique*

Endocrinology ◽  
1984 ◽  
Vol 114 (2) ◽  
pp. 629-637 ◽  
Author(s):  
RICHARD L. ECKERT ◽  
ALAKA MULLICK ◽  
ELLEN A. RORKE ◽  
BENITA S. KATZENELLENBOGEN
2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Mariana A. Callero ◽  
Andrea I. Loaiza-Pérez

Many estrogen-receptor- (ER-) expressing breast cancers become refractory to ER-based therapies. New antitumor drugs like aminoflavone (AF) and benzothiazoles (Bzs) have been developed and have exquisite antitumor activity in ER+MCF-7 and T47D cells and in a MCF-7 nude mouse model. ER(−) breast cancer cells like MDA-MB-231 are less susceptible. We previously found in MCF-7 cells that these drugs activate the aryl hydrocarbon receptor (AhR) via translocation to the nucleus, induction of AhR-specific DNA binding activity, and expression of CYP1A1, whose transcription is controlled by the AhR-ARNT transcription factor. CYP1A1 metabolizes AF and Bz to a species which directly or after further metabolism damages DNA. In contrast an AhR-deficient variant of MCF-7 or cells with predominantly nuclear AhR expression, such as MDA-MB 231, are resistant. Thus, these drugs, unlike other neoplastic agents, require AhR-mediated signaling to cause DNA damage. This is a new treatment strategy for breast cancers with intact AhR signaling.


1996 ◽  
Vol 57 (3-4) ◽  
pp. 203-213 ◽  
Author(s):  
Manuel Borrás ◽  
Ioanna Laios ◽  
Abdelhamid El Khissiin ◽  
Hye-Sook Seo ◽  
France Lempereur ◽  
...  

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