Overexpression of basic fibroblast growth factor (FGF–2) downregulates Bcl–2 and promotes apoptosis in MCF–7 human breast cancer cells

1999 ◽  
Vol 56 (2) ◽  
pp. 151-165 ◽  
Author(s):  
Paul Maloof ◽  
Qin Wang ◽  
Huisheng Wang ◽  
Dana Stein ◽  
Thomas N. Denny ◽  
...  
FEBS Letters ◽  
2000 ◽  
Vol 478 (3) ◽  
pp. 209-215 ◽  
Author(s):  
Anne-Sophie Vercoutter-Edouart ◽  
Jérôme Lemoine ◽  
Chanel E. Smart ◽  
Victor Nurcombe ◽  
Bénoni Boilly ◽  
...  

1994 ◽  
Vol 225 (3) ◽  
pp. 1041-1046 ◽  
Author(s):  
Sadakazu Miyashita ◽  
Masao Hirota ◽  
Toshiya Yamamoto ◽  
Chiyoka Shiroyama ◽  
Yoshiko Furukawa ◽  
...  

2000 ◽  
Vol 273 (2) ◽  
pp. 675-680 ◽  
Author(s):  
Alex Lyakhovich ◽  
Nickolai Aksenov ◽  
Pasi Pennanen ◽  
Susanna Miettinen ◽  
Merja H. Ahonen ◽  
...  

2005 ◽  
Vol 153 (4) ◽  
pp. 613-625 ◽  
Author(s):  
Andreas R Günthert ◽  
Carsten Gründker ◽  
Agnes Olota ◽  
Julia Läsche ◽  
Nicola Eicke ◽  
...  

About 50–64% of human breast cancers express receptors for GnRH-I. Direct antiproliferative effects of analogs of GnRH-I on human breast cancer cell lines have been shown. They are at least in part mediated by antagonizing growth promoting effects of estradiol, epidermal growth factor (EGF) or insulin-like growth factor. Recently, expression of a putative receptor for GnRH-II in human tissues was demonstrated. Antiproliferative effects of GnRH-II in human endometrial and ovarian cancer cells were shown not to be mediated through the GnRH-I receptor. Now we demonstrate direct anti-proliferative effects of the GnRH-I analog Triptorelin and the GnRH-II analog [d-Lys6]GnRH-II in MCF-7 and T47D human breast cancer cells expressing GnRH-I receptors and putative GnRH-II receptors. Pretreatment with Triptorelin or [d-Lys6]GnRH-II blocked EGF-induced autophosphoryla-tion of EGF receptor and activation of mitogen-activated protein kinase (extracellular-signal-regulated kinase 1/2 (ERK1/2)) in these cells. In sublines of MCF-7 and T47D cells, which were developed to be resistant to 4OH-tamoxifen, HER-2/p185 was overexpressed. Pretreatment of these cell lines with Triptorelin or [d-Lys6]GnRH-II completely abolished resistance to 4OH-tamoxifen, assessed by 4OH-tamoxifen-induced apoptosis. Analogs of GnRH-I and GnRH-II counteract EGF-dependent signal transduction in human breast cancer cells with expression of receptors for GnRH-I and GnRH-II. Through this mechanism, they probably reverse acquired resistance to 4OH-tamoxifen mediated through overexpression or activation of receptors of the c-erbB family.


2004 ◽  
Vol 64 (6) ◽  
pp. 2229-2237 ◽  
Author(s):  
Ho-Seong Kim ◽  
Angela R. Ingermann ◽  
Junko Tsubaki ◽  
Stephen M. Twigg ◽  
Gillian E. Walker ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document