| BackgroundIn 1971, Folkman first reported that the growth and metastatic spread of solid tumors are dependent on angiogenesis, and the chemical signal from tumor tissues is able to activate the resting vascular endothelial cells. Of the numerous promoters of angiogenesis that have been identified, one of the most importance is vascular endothelial growth factor(VEGF), which can modulate vascular permeability and promote endothelial cells fissiparism. VEGF can accelerate the proliferation of the vascular endothelial cells, stimulate the differentiation and anastomosis of capillary, then to develop the blood supply which is essential for the growth of and the nutrition delivery of solid tumors. A lot of evidence suggests that the VEGF expression is increased in malignant and the level of VEGF mRNA is positive correlated with the tumor microvessel density. Therefore, many scholars hope to inhibit tumor angiogenesis by VEGF blocking, so as to control the progressive growth of tumor. And they had made succeed in the experiment of2001animals. Like the other solid tumor, the growth and development of the ovarian cancer are correlated with its angiogenesis. It has been proved that the ovarian carcinoma express VEGF protein, either in vitro or in vivo. These findings suggest that blockade of VEGF may be an efficient strategy to inhibit formation of tumor angiogenesis and growth of ovarian cancer.Interferon gamma (IFN- v) is one of the commonest inflammatory cytokine, and has mulriple biological function. It has been applied in a broad field, involving the cancer therapy. It is also a common adjuvant therapy following surgery or chemotherapy in ovarian cancer. In the past years, it was thought that the primary anticancer function of IFN-y was only to inhibit some tumor cells proliferation and modulate the immunoreaction. Recently, some research found that IFN- y even could inhibit the angiogenesis in cancer. But the mechanism of its' antiangiogenesis remains uncertain, and no report is found on whether it is occurs in ovarian cancer.I IFN- y effects on the expression of VEGF in ovarian carcinoma cell lines (SKOV3). Objective: To determine whether the antiangiogenesis of IFN- y in ovarian cancer is induced by depressing the expression of VEGF mRNA and protein by means of observing affect of IFN-y on SKOV3 in both DMA and protein lever. Methods: 1. The morphological changes and proliferation of SKOV3 during treating with IFN- y were observed through inverted phase-contrast microscope and by MTT method respectively. 2. Affect of IFN-y on expression of VEGF mRNA in SKOV3 culture is determined by relative quantitative RT-PCR. 3. The VEGF protein level in supernatants of SKOV3 is determined by enzyme-linked immunosorbentassay(ELISA). 4. Expression of VEGF protein in the IFN- y treated and the control group was observed using immunocytochemical staining. All the data were statistically managed with SPSS 8.0 for windows. Results: 1. Compared with the control, the SKOV3 cells grew well after treatment of IFN-Y , and there hardly were any dead cells. But the number of antennae in the cells increased a little. 2. There was no change of SKOV3 cells proliferation during treating with different concentrations (l~10000U/ml) or time (0~60h) (P>0. 05). It was suggested that IFN-Y couldn't affect the growth of SKOV3. 3. Treatment of IFN- Y could decrease expression of VEGF mRNA in SKOV3(p<0.01). At the concentration of 10U/ml, the inhibition appeared. Following the concentration increasing, the inhibit rate increased(5. 19 + 0. 62, 15.6 ?.11, 21.62 + 2.56, 22.39 + 1.73). At the concentration of lOOOU/ml, the inhibit rate reached the maximum. Further increasing the concentration did not enhanced of the inhibition. Whereas,there was no positive correlation between the time and the inhibition. The inhibition didn't appear until the cells exposed to IFN- Y for 24h. Thereafter increasing of inhibition also did not follow extending the time. 4. IFN- Y decreased the level of VEGF protein in supernatants of SKOV3 cult...
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