scholarly journals Co-regulated gene expression by oestrogen receptor α and liver receptor homolog-1 is a feature of the oestrogen response in breast cancer cells

2013 ◽  
Vol 41 (22) ◽  
pp. 10228-10240 ◽  
Author(s):  
Chun-Fui Lai ◽  
Koen D. Flach ◽  
Xanthippi Alexi ◽  
Stephen P. Fox ◽  
Silvia Ottaviani ◽  
...  
2004 ◽  
Vol 21 (2) ◽  
pp. 134-144 ◽  
Author(s):  
A. G. Recchia ◽  
A. Vivacqua ◽  
S. Gabriele ◽  
A. Carpino ◽  
G. Fasanella ◽  
...  

2020 ◽  
Vol 511 ◽  
pp. 110859 ◽  
Author(s):  
Sean M. Holloran ◽  
Bakhtiyor Nosirov ◽  
Katherine R. Walter ◽  
Gloria M. Trinca ◽  
Zhao Lai ◽  
...  

2014 ◽  
Vol 465 (1) ◽  
pp. 49-61 ◽  
Author(s):  
Brandie N. Radde ◽  
Margarita M. Ivanova ◽  
Huy Xuan Mai ◽  
Joshua K. Salabei ◽  
Bradford G. Hill ◽  
...  

Oestrogen receptor α-expressing breast cancer cells show differences in basal bioenergetics profiles and bioenergetics responses to serum depletion, oestradiol and tamoxifen as measured in real time by extracellular flux analysis in intact cells.


BMC Cancer ◽  
2014 ◽  
Vol 14 (1) ◽  
Author(s):  
María F Montenegro ◽  
María del Mar Collado-González ◽  
María Piedad Fernández-Pérez ◽  
Manel B Hammouda ◽  
Lana Tolordava ◽  
...  

2003 ◽  
Vol 179 (1) ◽  
pp. 41-53 ◽  
Author(s):  
R Margueron ◽  
A Licznar ◽  
G Lazennec ◽  
F Vignon ◽  
V Cavailles

We analysed the antiproliferative activity of various histone deacetylase (HDAC) inhibitors such as trichostatin A (TSA) on human breast cancer cells. We observed a lower sensitivity to HDAC inhibition for oestrogen receptor negative (ER-) versus positive (ER+) cell lines. This differential response was associated neither with a modification of drug efflux via the multidrug resistance system nor with a global modification of histone acetyltransferase (HAT)/HDAC activities. In contrast, we demonstrated that in ER+ breast cancer cells the p21(WAF1/CIP1) gene was more sensitive to TSA regulation and was expressed at higher levels. These differences were observed both in transient transfection experiments and on the endogenous p21(WAF1/CIP1) gene. The Sp1 transcription factor, which was shown to interact in vitro with both class I and class II HDACs, is sufficient to confer the differential sensitivity to TSA and participated in the control of p21(WAF1/CIP1) basal expression. Finally, re-expression of ERalpha following adenoviral infection of ER- breast cancer cells increased both p21(WAF1/CIP1) protein accumulation and the growth inhibitory activity of TSA. Altogether, our results highlight the key role of ERalpha and p21(WAF1/CIP1) gene expression in the sensitivity of breast cancer cells to hyperacetylating agents.


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