Platelet-activating factor (PAF) is a lipid mediator that stimulates the in vitro growth of various human tumour cell lines and that enhances the effect of vascular endothelial growth factor that plays a key role during angiogenesis of human cancer.
Within ovarian carcinomas, the percentage of VEGF-positive cells was significantly associated with the grade of cancer but not with cancer cell types or cancer stages.
Because VEGF can promote neovascularization in cancer cells, an induction of VEGF by at-RA may preclude the therapeutic application of at-RA to cancer patients.
The expression of vascular endothelial growth factor in cancer cells, which could be blocked by dactinomycin, were increased to a certain degree, while the relative half-life of VEGF mRNA was not prolonged after treatment with hydrogen peroxide.
Our results suggest that increased DNA instability, enhanced proliferative activity, p53 mutation, and induction of DFF45 and VEGF may allow cancer cell proliferation, enhance their survival by escaping apoptosis, and provide abundant nutrients during early-stage carcinogenesis of oral leukoplakia.
A recent report that anti-VEGF antibody reduced cancer growth in nude mice transplanted with human thyroid carcinoma is an indication this field holds for future studies.
Previously, we demonstrated the significance of vascular endothelial growth factor (VEGF) in promoting the growth of tetracycline-regulated human VEGF165 retroviral vector transduced T47-D breast carcinoma cells, particularly at the early stages of tumor development (Cancer Res.57 (1997) 3924).
Furthermore, while the efficiency of the IRES from the vascular endothelium growth factor gene was not significantly higher than the EMCV IRES under normoxic conditions, expression was significantly increased under hypoglycemic conditions, suggesting that the VEGF IRES could be exploited in cancer gene therapy to preferentially target expression of therapeutic genes at the relatively hypoglycemic cores of tumors.
Taken together, these findings suggest that the overexpression of cyclin D1 can confer esophageal cancer cells with enhanced malignancy through increases in anchorage-independent growth and VEGF production, and down-regulation of Fas expression, thus suggesting novel functions of the cyclin D1 protein in tumor progression.
Furthermore, the level of vascular endothelial growth factor in sera from six cancer patients was significantly diminished 2-3 weeks after completion of whole-body hyperthermia at 42 degrees C (49.9+/-36.5 pg x ml(-1), P<0.01) as compared with that prior to the treatment (177.0+/-77.5 pg x ml(-1)).
We have shown that a soluble receptor for vascular endothelial growth factor (sVEGFR), which adsorbs VEGF and may function as a dominant-negative receptor, suppresses tumor angiogenesis and enhances apoptosis of cancer cells, thereby inhibiting tumor growth [Cancer Res 60 (2000) 2169-2177].
To examine the hypoxia responsiveness of the VEGF promoter, lung cancer cells were transiently exposed to hypoxia; this treatment increased enhanced green fluorescent protein (EGFP) expression after AdVEGFEGFP infection in both normal and cancer cell lines, and enhanced apoptosis and decreased the number of surviving cancer cells compared with the Ad/BAX plus Ad/Cre binary adenoviral system.
Vascular endothelial growth factor (VEGF) plays a critical role during normal embryonic angiogenesis and also in the pathological angiogenesis that occurs in a number of diseases, including cancer.
The transcript levels for the different VEGF-A splice variants (VEGF(121), VEGF(165), VEGF(189)) were at least 10-fold higher in the cancer cases, with the highest levels in the primary tumours demonstrating lympho-vascular space involvement.
The VEGF189 molecule, which is strongly bound to the cell surface, has unique properties and high potential in local angiogenesis and tumor growth in the cancer inductive microenvironment.
A significant correlation was also found between iNOS and VEGF expression (P = 0.001). iNOS activity and cyclic GMP production were significantly higher in the cancer specimens than in the normal mucosa (P < 0.0001 and P < 0.0001, respectively), as well as in metastatic tumors than in nonmetastatic ones (P = 0.002 and P = 0.04, respectively).
A significant correlation in the expression ratios between LPA(2) or LPA(3) and VEGF was found (gamma=0.617, P<0.0001; gamma=0.431, P<0.001) in patients with cancer.