α-Mangostin-induced apoptosis is mediated by estrogen receptor α in human breast cancer cells

2014 ◽  
Vol 66 ◽  
pp. 158-165 ◽  
Author(s):  
Yeong-Seon Won ◽  
Ju-Hye Lee ◽  
Soon-Jae Kwon ◽  
Jae-Yong Kim ◽  
Ki-Hun Park ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Α ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Induced Apoptosis

Estrogen receptor-α regulates SOCS-3 expression in human breast cancer cells

2005 ◽  
Vol 335 (1) ◽  
pp. 168-174 ◽  
Author(s):  
Jason Matthews ◽  
Tova Almlöf ◽  
Silke Kietz ◽  
Jörg Leers ◽  
Jan-Åke Gustafsson
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Α ◽  
Human Breast Cancer Cells ◽  
Human Breast

scholarly journals Inflammatory macrophage derived TNFα downregulates estrogen receptor α via FOXO3a inactivation in human breast cancer cells

2020 ◽  
Vol 390 (1) ◽  
pp. 111932
Author(s):  
Frida Björk Gunnarsdóttir ◽  
Catharina Hagerling ◽  
Caroline Bergenfelz ◽  
Meliha Mehmeti ◽  
Eva Källberg ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Α ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Inflammatory Macrophage

scholarly journals The Aryl Hydrocarbon Receptor Mediates Degradation of Estrogen Receptor α through Activation of Proteasomes

2003 ◽  
Vol 23 (6) ◽  
pp. 1843-1855 ◽  
Author(s):  
Mark Wormke ◽  
Matthew Stoner ◽  
Bradley Saville ◽  
Kelcey Walker ◽  
Maen Abdelrahim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Α ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Aryl Hydrocarbon

ABSTRACT 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and other aryl hydrocarbon receptor (AhR) ligands suppress 17β-estradiol (E)-induced responses in the rodent uterus and mammary tumors and in human breast cancer cells. Treatment of ZR-75, T47D, and MCF-7 human breast cancer cells with TCDD induces proteasome-dependent degradation of endogenous estrogen receptor α (ERα). The proteasome inhibitors MG132, PSI, and PSII inhibit the proteasome-dependent effects induced by TCDD, whereas the protease inhibitors EST, calpain inhibitor II, and chloroquine do not affect this response. ERα levels in the mouse uterus and breast cancer cells were significantly lower after cotreatment with E plus TCDD than after treatment with E or TCDD alone, and our results indicate that AhR-mediated inhibition of E-induced transactivation is mainly due to limiting levels of ERα in cells cotreated with E plus TCDD. TCDD alone or in combination with E increases formation of ubiquitinated forms of ERα, and both coimmunoprecipitation and mammalian two-hybrid assays demonstrate that TCDD induces interaction of the AhR with ERα in the presence or absence of E. In contrast, E does not induce AhR-ERα interactions. Thus, inhibitory AhR-ERα cross talk is linked to a novel pathway for degradation of ERα in which TCDD initially induces formation of a nuclear AhR complex which coordinately recruits ERα and the proteasome complex, resulting in degradation of both receptors.

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