Induction of vascular endothelial growth factor by peptidyl-prolyl isomerase Pin1 in breast cancer cells

2008 ◽  
Vol 369 (2) ◽  
pp. 547-553 ◽  
Author(s):  
Mi Ra Kim ◽  
Hong Seok Choi ◽  
Tae-Hwe Heo ◽  
Sun Wook Hwang ◽  
Keon Wook Kang
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Vascular Endothelial ◽  
Prolyl Isomerase ◽  
Peptidyl Prolyl Isomerase ◽  
Endothelial Growth Factor

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

scholarly journals Vascular endothelial growth factor induces proliferation of breast cancer cells and inhibits the anti-proliferative activity of anti-hormones

2006 ◽  
Vol 13 (3) ◽  
pp. 905-919 ◽  
Author(s):  
Yayun Liang ◽  
Rolf A Brekken ◽  
Salman M Hyder
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Vascular Endothelial ◽  
Ru 486 ◽  
Endothelial Growth Factor

Increased levels of vascular endothelial growth factor (VEGF) are associated with a poor response of breast cancer to anti-hormone treatment. Although VEGF is regarded as an endothelial-specific growth factor, recent reports have shown that VEGF can promote proliferation of other cell types, including breast tumor cells. We have characterized the proliferative effects of VEGF in breast cancer cell lines that are commonly used for understanding the role of estrogens, progestins, and anti-hormones on tumor growth. Since steroid hormones can increase the level of VEGF in certain breast cancer cells, we evaluated the effects of exogenous VEGF on the growth-suppressive effects of anti-estrogen (ICI 182,780) and RU-486 (anti-progestin mifepristone) in human breast cancer cells. VEGF165 and VEGF121 increased the proliferation of tumor cell lines that expressed VEGFR-2 (VEGF receptor 2) (flk/kdr) via the extracellular signal-regulated kinase/mitogen activated protein kinase (ERK/MAPK) pathway. Furthermore, VEGF induced the expression of the anti-apoptotic protein Bcl-2 and blocked down-regulation of Bcl-2 by ICI 182,780 and induced Bcl-2 in BT-474 and T47-D cells even in the presence of RU-486. Increased Bcl-2 levels in response to VEGF were associated with increased proliferation and survival of tumor cells even in the presence of anti-hormones. These results suggest that VEGF stimulates proliferation of VEGFR2-positive tumor cells, promotes survival via the expression and activity of Bcl-2 and overrides the growth-suppressive effects of anti-hormones. This represents a potential explanation for anti-hormone resistance and tumor progression in clinical samples. Thus, it may be useful to use combined modality treatment involving anti-hormones and anti-angiogenic agents to treat breast cancers that express elevated levels of VEGF.

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