scholarly journals The Polycomb group protein RING1B is overexpressed in ductal breast carcinoma and is required to sustain FAK steady state levels in breast cancer epithelial cells

Oncotarget ◽  
2014 ◽  
Vol 5 (8) ◽  
pp. 2065-2076 ◽  
Author(s):  
Almudena Bosch ◽  
Konstantina Panoutsopoulou ◽  
Josep Maria Corominas ◽  
Ramón Gimeno ◽  
Gema Moreno-Bueno ◽  
...  
Neoplasia ◽  
2005 ◽  
Vol 7 (11) ◽  
pp. 1011-1019 ◽  
Author(s):  
Michael Zeidler ◽  
Sooryanarayana Varambally ◽  
Qi Cao ◽  
Arul M. Chinnaiyan ◽  
David O. Ferguson ◽  
...  

2010 ◽  
Vol 25 (4) ◽  
pp. 199-205 ◽  
Author(s):  
Lei Li ◽  
Lu Lu ◽  
Xiang Lü ◽  
Xue-song Wu ◽  
De-pei Liu ◽  
...  

2007 ◽  
Vol 27 (14) ◽  
pp. 5105-5119 ◽  
Author(s):  
Bin Shi ◽  
Jing Liang ◽  
Xiaohan Yang ◽  
Yan Wang ◽  
Youna Zhao ◽  
...  

ABSTRACT Essential for embryonic development, the polycomb group protein enhancer of zeste homolog 2 (EZH2) is overexpressed in breast and prostate cancers and is implicated in the growth and aggression of the tumors. The tumorigenic mechanism underlying EZH2 overexpression is largely unknown. It is believed that EZH2 exerts its biological activity as a transcription repressor. However, we report here that EZH2 functions in gene transcriptional activation in breast cancer cells. We show that EZH2 transactivates genes that are commonly targeted by estrogen and Wnt signaling pathways. We demonstrated that EZH2 physically interacts directly with estrogen receptor α and β-catenin, thus connecting the estrogen and Wnt signaling circuitries, functionally enhances gene transactivation by estrogen and Wnt pathways, and phenotypically promotes cell cycle progression. In addition, we identified the transactivation activity of EZH2 in its two N-terminal domains and demonstrated that these structures serve as platforms to connect transcription factors and the Mediator complex. Our experiments indicated that EZH2 is a dual function transcription regulator with a dynamic activity, and we provide a mechanism for EZH2 in tumorigenesis.


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