Here by comparing cell proliferation status before and after transfection, we found that cell proliferation Compound C ic50 after gene transfection was accelerated. To further test the role of Lewis y in ovarian cancer cell proliferation, we treat Lewis y-overexpressing RMG-I-H ovarian cancer cells with α-L-fucosidase for the first time, which reducing the content of fucosylated antigens on cell surface. Through observing biological behaviors

of cell before and after α-L-fucosidase treatment, we found the cell proliferation rate in transfected group was significantly higher than that of α-L-fucosidase-treatment group. Our preliminary study proved that the lactose type I chain family of the original RMG-I cells was Trichostatin A in vitro primarily glycolipid, and they were Lc4Cer, Lewis a, and Lewis b, whereas, H-1 instead had the absolute

domination in the successfully transfected cells. For the glycolipids of the lactose type II chain family, such as Lewis x, Lewis y, IV3NeuAc-nLc4Cer and NeuAc-LeX, their concentrations were over 0.01 μg per milliliter of dry cells; however, the glycolipids shown in the transfected RMG-I-H cells were Lewis x and Lewis y. 42.6% of Lewis x in the RMG-I-H was converted into Lewis y, which was in much higher percentage than the 3.2% of the original RMG-I cells. Although type I chain family H-1 had the absolute domination in the transfected RMG-I-H Selonsertib supplier cells, its actual content was only 1/4 of the Lewis y [8]. These further proved that the changes of biological behaviors of RMG-I-H cells, such as enhancement of proliferation and growth, as well as the worsening in the Interleukin-2 receptor severity of malignancy, all had to do with the increase in Lewis y antigen. Blocking experiments

with Lewis y specific monoclonal antibody provided further evidence for its function. The molecular mechanism by which Lewis y antigen causes the malignancy of ovarian cancer cell have not been completely understood. In previous studies, we tested the differences in oncogene expression before and after α1,2-FT gene transfection using gene chips technology. Results showed that: there were 88 differentially expressed genes after cell transfection, and altered genes mainly involved these genes regulating cell proliferation, signal transduction, transcription and so on [25]. Thus, it is possible that Lewis y may be an important component in signaling transduction pathway participating in signal transduction inside cell and further promoting proliferation of ovarian cancer cells. Studies found that anti-Lewis y antibodies (ABL364 and IGN311) blocked the activation of mitogen-activated protein kinase (MAPK) signaling pathway in A431 cells and prevented cell proliferation [26]. The MAPK signaling pathway has central roles in the regulation of cell survival and proliferation and our experimental results have further verified this conclusion.