Correlation between the expression of aquaporin 1 and hypoxia-inducible factor 1 in breast cancer tissues

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Shiying Yu ◽  
Liang Xiao ◽  
Jun Zhang ◽  
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2010 ◽  
Vol 1 (4) ◽  
pp. 657-662 ◽  
Author(s):  
YONGHONG SHI ◽  
MIAOMIAO CHANG ◽  
FANG WANG ◽  
XIAOHUI OUYANG ◽  
YONGFENG JIA ◽  
...  

2016 ◽  
Vol Volume 9 ◽  
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Fangfang Lai ◽  
qian liu ◽  
xiaoyu liu ◽  
Ming Ji ◽  
Ping Xie ◽  
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2014 ◽  
Vol 13 (1) ◽  
pp. 12 ◽  
Author(s):  
Khaled Ghattass ◽  
Sally El-Sitt ◽  
Kazem Zibara ◽  
Saide Rayes ◽  
Makhluf J Haddadin ◽  
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2011 ◽  
Vol 286 (12) ◽  
pp. 10773-10782 ◽  
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Ernestina Marianna De Francesco ◽  
Adele Vivacqua ◽  
Diego Sisci ◽  
Maria Luisa Panno ◽  
...  

GPR30, also known as GPER, has been suggested to mediate rapid effects induced by estrogens in diverse normal and cancer tissues. Hypoxia is a common feature of solid tumors involved in apoptosis, cell survival, and proliferation. The response to low oxygen environment is mainly mediated by the hypoxia-inducible factor named HIF-1α, which activates signaling pathways leading to adaptive mechanisms in tumor cells. Here, we demonstrate that the hypoxia induces HIF-1α expression, which in turn mediates the up-regulation of GPER and its downstream target CTGF in estrogen receptor-negative SkBr3 breast cancer cells and in HL-1 cardiomyocytes. Moreover, we show that HIF-1α-responsive elements located within the promoter region of GPER are involved in hypoxia-dependent transcription of GPER, which requires the ROS-induced activation of EGFR/ERK signaling in both SkBr3 and HL-1 and cells. Interestingly, the apoptotic response to hypoxia was prevented by estrogens through GPER in SkBr3 cells. Taken together, our data suggest that the hypoxia-induced expression of GPER may be included among the mechanisms involved in the anti-apoptotic effects elicited by estrogens, particularly in a low oxygen microenvironment.


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