Differential dependency of human cancer cells on vascular endothelial growth factor-mediated autocrine growth and survival

2011 ◽  
Vol 309 (2) ◽  
pp. 145-150 ◽  
Author(s):  
Jungwhoi Lee ◽  
Jungsul Lee ◽  
Hana Yu ◽  
Kyungsun Choi ◽  
Chulhee Choi
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Human Cancer ◽  
Vascular Endothelial ◽  
Autocrine Growth ◽  
Growth And Survival ◽  
Human Cancer Cells ◽  
Endothelial Growth Factor

scholarly journals Regulation of vascular endothelial growth factor expression by acidosis in human cancer cells

Oncogene ◽  
2001 ◽  
Vol 20 (28) ◽  
pp. 3751-3756 ◽  
Author(s):  
Qian Shi ◽  
Xiangdong Le ◽  
Bailiang Wang ◽  
James L Abbruzzese ◽  
Qinghua Xiong ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Human Cancer ◽  
Vascular Endothelial ◽  
Human Cancer Cells ◽  
Factor Expression ◽  
Growth Factor Expression ◽  
Endothelial Growth Factor

A novel approach for the discrimination of culture medium from Vascular Endothelial Growth Factor (VEGF) overexpressing colorectal cancer cells

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Sinem Tunçer ◽  
Rafig Gurbanov
Keyword(s):  
Colorectal Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Ftir Spectroscopy ◽  
Cancer Cells ◽  
Lower Amount ◽  
Vascular Endothelial ◽  
Colorectal Cancer Cells ◽  
Endothelial Growth Factor

AbstractObjectivesThe expression level of Vascular Endothelial Growth Factor (VEGF) is assumed as a prognostic marker for several tumor types, including colorectal cancer. Therefore, the determination of pre- and post-therapy levels of VEGF appears to have great value in the assessment of tumor prognosis. Enzyme-Linked Immunosorbent Assay (ELISA) is commonly used for the determination of serum or plasma VEGF levels, but the method is costly and time-consuming. In this study, we aimed to describe a rapid and cost-effective analysis method to discriminate VEGF overexpressing colorectal cancer-derived conditioned medium (CM).MethodsAttenuated Total Reflection (ATR)-Fourier Transform Infrared (FTIR) spectroscopy, combined with Principal Component Analysis (PCA) and Linear Discriminant Analysis (LDA), was used to differentiate VEGF overexpressing colorectal cancer cell line CM from CM obtained from the corresponding control cells which express and secrete relatively lower amount of VEGF.ResultsSamples belong to VEGF overexpressing colorectal cancer cells were clearly distinguished from the control group with very high PC scores as PC1 + PC2 = 96%. Besides, a 100% accurate distinction between these two groups was achieved by the LDA analysis.ConclusionsATR-FTIR spectroscopy combined with pattern recognition techniques was able to discriminate CM of VEGF overexpressing colorectal cancer cells with high efficiency and accuracy.

scholarly journals HER2 (neu) Signaling Increases the Rate of Hypoxia-Inducible Factor 1α (HIF-1α) Synthesis: Novel Mechanism for HIF-1-Mediated Vascular Endothelial Growth Factor Expression

2001 ◽  
Vol 21 (12) ◽  
pp. 3995-4004 ◽  
Author(s):  
Erik Laughner ◽  
Panthea Taghavi ◽  
Kelly Chiles ◽  
Patrick C. Mahon ◽  
Gregg L. Semenza
Keyword(s):  
Breast Cancer ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cancer Cells ◽  
Half Life ◽  
Hypoxia Inducible Factor ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Her2 Signaling ◽  
Endothelial Growth Factor

ABSTRACT Hypoxia-inducible factor 1 (HIF-1) is a transcriptional activator composed of HIF-1α and HIF-1β subunits. Several dozen HIF-1 targets are known, including the gene encoding vascular endothelial growth factor (VEGF). Under hypoxic conditions, HIF-1α expression increases as a result of decreased ubiquitination and degradation. The tumor suppressors VHL (von Hippel-Lindau protein) and p53 target HIF-1α for ubiquitination such that their inactivation in tumor cells increases the half-life of HIF-1α. Increased phosphatidylinositol 3-kinase (PI3K) and AKT or decreased PTEN activity in prostate cancer cells also increases HIF-1α expression by an undefined mechanism. In breast cancer, increased activity of the HER2 (also known as neu) receptor tyrosine kinase is associated with increased tumor grade, chemotherapy resistance, and decreased patient survival. HER2 has also been implicated as an inducer of VEGF expression. Here we demonstrate that HER2 signaling induced by overexpression in mouse 3T3 cells or heregulin stimulation of human MCF-7 breast cancer cells results in increased HIF-1α protein and VEGF mRNA expression that is dependent upon activity of PI3K, AKT (also known as protein kinase B), and the downstream kinase FRAP (FKBP-rapamycin-associated protein). In contrast to other inducers of HIF-1 expression, heregulin stimulation does not affect the half-life of HIF-1α but instead stimulates HIF-1α synthesis in a rapamycin-dependent manner. The 5′-untranslated region of HIF-1α mRNA directs heregulin-inducible expression of a heterologous protein. These data provide a molecular basis for VEGF induction and tumor angiogenesis by heregulin-HER2 signaling and establish a novel mechanism for the regulation of HIF-1α expression.

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