Effect of 17β-estradiol, progesterone, synthetic progestins, tibolone, and tibolone metabolites on vascular endothelial growth factor mRNA in breast cancer cells

2005 ◽  
Vol 84 (2) ◽  
pp. 485-491 ◽  
Author(s):  
Sebastian Mirkin ◽  
Benjamin C. Wong ◽  
David F. Archer
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Vascular Endothelial ◽  
17Β Estradiol ◽  
Endothelial Growth Factor

scholarly journals Vascular Endothelial Growth Factor Receptor-2 Expression Is Induced by 17β-Estradiol in ZR-75 Breast Cancer Cells by Estrogen Receptor α/Sp Proteins

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3285-3295 ◽  
Author(s):  
Kelly J. Higgins ◽  
Shengxi Liu ◽  
Maen Abdelrahim ◽  
Kyungsil Yoon ◽  
Kathryn Vanderlaag ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Chromatin Immunoprecipitation ◽  
Breast Cancer Cells ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Rich Region ◽  
17Β Estradiol ◽  
Endothelial Growth Factor

Vascular endothelial growth factor receptor-2 kinase insert domain receptor (VEGFR2/KDR) is critical for angiogenesis, and VEGFR2 mRNA and protein are expressed in ZR-75 breast cancer cells and induced by 17β-estradiol (E2). Deletion analysis of the VEGFR2 promoter indicates that the proximal GC-rich region is required for both basal and hormone-induced transactivation, and mutation of one or both of the GC-rich motifs at −58 and −44 results in loss of transactivation. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that Sp1, Sp3, and Sp4 proteins bind the GC-rich region of the VEGFR2 promoter. Results of the chromatin immunoprecipitation assay also demonstrate that ERα is constitutively bound to the VEGFR2 promoter and that these interactions are not enhanced after treatment with E2, whereas ERα binding to the region of the pS2 promoter containing an estrogen-responsive element is enhanced by E2. RNA interference studies show that hormone-induced activation of the VEGFR2 promoter constructs requires Sp3 and Sp4 but not Sp1, demonstrating that hormonal activation of VEGFR2 involves a nonclassical mechanism in which ERα/Sp3 and ERα/Sp4 complexes activate GC-rich sites where Sp proteins but not ERα bind DNA. These results show for the first time that Sp3 and Sp4 cooperatively interact with ERα to activate VEGFR2 and are in contrast to previous results showing that several hormone-responsive genes are activated by ERα/Sp1 in breast cancer cell lines.

scholarly journals Up-regulation of Vascular Endothelial Growth Factor C in Breast Cancer Cells by Heregulin-β1

2002 ◽  
Vol 278 (8) ◽  
pp. 5750-5759 ◽  
Author(s):  
Pei-Wen Tsai ◽  
Shine-Gwo Shiah ◽  
Ming-Tsan Lin ◽  
Cheng-Wen Wu ◽  
Min-Liang Kuo
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Vascular Endothelial ◽  
Factor C ◽  
Endothelial Growth Factor

Decreased production of vascular endothelial growth factor in adriamycin-resistant breast cancer cells

2008 ◽  
Vol 268 (2) ◽  
pp. 225-232 ◽  
Author(s):  
Jung-Ae Kim ◽  
Kyoung Bin Cho ◽  
Mi Ra Kim ◽  
Byung Chul Park ◽  
Sang Kyum Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor
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