Effects of Interferon-α on Vascular Endothelial Growth Factor and E-cadherin Expression in Liver Cancer Cell Lines

• Main Authors: Shu-Bauh Hu, 胡淑寶
• Other Authors: Chen-Guo Ker
• Format: Others
• Language: zh-TW
• Published: 2004
• Online Access: http://ndltd.ncl.edu.tw/handle/27512200453751108473

碩士 === 高雄醫學大學 === 藥學研究所碩士在職專班 === 92 === Purpose: Vascular endothelial growth factor(VEGF) and E-cadherin have been examined and taken for indicators of angiogenesis and metastasis respectively. In our study, we evaluated the in vitro effects of IFN-α treatment on the tumorigenicity of liver cancer cell lines. From the changes of the expression of VEGF and E-cadherin, we expected to evaluate the prognostic markers. Materials and Methods: Two well differentiated (Hep G2, Hep 3B) and one poor differentiated (SK-Hep I) human liver cancer lines were used. Cells were incubated with Interferon-α to evaluate their metastatic potential. Hep G2, SK-Hep-I cells were incubated with IFN-α for different concentrations (5000 unit/ml; 1000 unit/ml) and different periods(3;6 days) of time. Then, the VEGF protein expression was assayed by ELISA test in those culture media. The Hep 3B cells were treated with fresh medium, that contained 1000, 5000, 20000 unit/ml INF-α. It were incubated for 3 days. After that, E-cadherin expression changes was confirmed by Western blotting and Immunocytochemistry. All three cell lines, treated with INF-α, their survival rates were measured by cell counting and MTT test . Results: In the angiogenesis study, both in group A(5000 unit/ml; 3days)and group B(1000 unit/ml, 6days), the VEGF protein expression was down-regulated by IFN-α. In Group A, the VEGF protein expression were, in Hep G2 (no IFN-α:124.4, with IFN-α: 76.8),and in SK-Hep-I (no IFN-α: 44.5, with IFN-α: 30.0). In Group B, VEGF protein expression were, in Hep G2 (no IFN-α: 225.5, with IFN-α:151.4) and SK-Hep-I (no IFN-α: 74.1, with IFN-α: 53.4). In the cell invasion study, Western blotting and Immunocytochemistry showed that E-cadherin expression were up-regulated by the increasing concentration of IFN-α. The declined cell number counts and survival rates of all three cell lines showed antiproliferative activity of IFN-α. Conclusion: IFN-α confers its antitumor activity, at least in part, by its antiangiogenic activity, which results from decreased VEGF expression, and by anti-invasive activity, which results from elevated E-cadherin expression and antiproliferative activity on cancer cell lines. The results may help us to design the treatment protocol and to define the chemopreventive role of IFN-α. Key words：Interferon-α，Angiogenesis，Invasion，Metastasis，VEGF，E-cadherin