Suppression Of FUT4 And PKCα Induces Cell Apoptosis Of A431 Cells

α1,3-fucosyltransferases(α1,3 FUT)participate in the fucosylation synthesis of Lewis oligosaccharide chains by transferring GDP-fucose to the terminal N-acetyllactosamine(GlcNAc)with theα1,3 orα1,4 linkage.α1,3 FUTs include FUT3, 4, 5, 6, 7 and 9 genes. Fucosyltransferase IV (FUT4) is an essential enzyme that catalyzes the synthesis of Lewis Y (LeY) by transferring GDP-fucose to the terminal N-acetylglucosamine(GlcNAc)with theα1,3-linkage. FUT4 is mainly expressed in leukocyte and some epithelial cells. FUT4 was found abnormally expressed, eg, gastric carcinoma, colorectal cancerous, pancreatic cancer, et al. Therefore, regulating the expression of fucosyltransferases may change the synthesis of LeY and affect the biological function of LeY.LeY antigen carried by the glycoproteins and glycolipids on cell surface, is a difucosylated oligosaccharide with the chemical structure [Fucα1→2Galβ1→4(Fucα1→3)GlcNAcβ1→R] . LeY is able to facilitate henogenesis, organ formation, cell differentiation, tumorigenesis et al. LeY has been recognized as a tumor-associated antigen in a variety of cancer process particularly in cell proliferation, invasion and metastasis, highly expressed LeY is found in the majority (70-90%) of human cancers of epithelial orogin.The previous work in our lab showed that the suppression of FUT4 by RNAi and LeY antibody could inhibit the A431 cell proliferation, the overpression of FUT4 could increase the synthesis of LeY and inhibit cell apoptosis. The effect of FUT4 on cell proliferation and cell apoptosis in A431 cells is not clearly elucidated. It is found that protien kinase C has an important role in the development and progress of cancers. PKCαas a targeted anti-cancer drugs has made significant progress in clinic trial. This work mainly explored the effect of FUT4 RNAi and PKCαas on cell apoptosis in A431 cells.