The role of alpha-fetoprotein in maintaining the growth of human hepatoma cells

14081 Background: This study was to explored the functional mechanism of alpha-fetoprotein (AFP) in maintaining the proliferation of human hepatoma cells line Bel 7402 and the immunsuppression of lymphocyte Jurkat cells. Methods: Western blot was used to detecting the expression of some apoptosis-related gene, fluorescence labeled AFP and confocal microscopy scanning for receptor binding assay in the membrane in Jurkat cells. Results: It showed that AFP could enhance the expression of survivin and c-ras, but restrain caspase-3 express in Bel 7402 cells by Western blotting analysis. It also showed that AFP could bind to the membrane of Jurkat cells by confocal microscopy scanning, and when treated Jurkat with AFP, it indicated that AFP could repress the expression of survivin and Livin and elevated the activity of caspase-3 in the cells; Co-cultured Bel 7402 cells with Jurkat cells, the expression of tumor necrosis related-apoptosis induced ligand (TRAIL) in Jurkt cells was inhibited, when pretreatment with monoclonal antibody of AFP (Anti-AFP), the restrained effect of TRAIL express and the activity of caspase-3 was elevated in Jurkat cells was removed. It also indicated that Anti-AFP had an ability to block these functions of AFP. Conclusions: AFP has a capability to promote the growth and escape from immune surveillance of human hepatoma cells through enhancing the expression of ras and survivin gene in Bel 7402 cells, suppressing TRAIL, survivin and Livin expressed and upregulated activity of caspase-3 in Jurkat cells. No significant financial relationships to disclose.