Therefore, we established a relationship between PSA expression on the surface of primary tumor cells and the metastatic process. When metastases occurred in endoneuraminidase-N injected animals, they strongly expressed PSA-NCAM. Endoneuraminidase-N also increased the delay in ascitic formation and decreased the number of lung or liver metastases in the case of intraperitoneal tumors but not in the case of intramuscular tumors. Repeated injections of endoneuraminidase-N led to a decrease in PSA expression in primary intraperitoneal nodules and ascites but not in intramuscular primary tumors. Mice with primary intramuscular tumors were taken as control. We found that NEU1 is highly expressed in immature GCs. To evaluate the putative role of PSA in the metastatic process we used a specific cleavage of PSA on NCAM by endoneuraminidase-N on intraperitoneal primary tumors. Developing a migration assay of immature GCs in vitro, we found that the pharmacological depletion of PSA prevents the migration of GCs, whereas the inhibition of PSA degradation with a neuraminidase inhibitor accelerates this migration. Intraperitoneal injections also induced peritoneal carcinosis, ascites, and liver metastases. B: Preincubation with the mitogen-activated protein kinase inhibitor PD98059 (PD) blocks the morphological differentiation induced by either endo N or BDNF. six sialic acid monomers (Vimr et al., 1984) attached to the core glycan. We observed the formation of lung metastases when TE671 cells were injected intravenously, intramuscularly, and intraperitoneally, but not subcutaneously. A: Endoneuraminidase (endo N) or BDNF (100 ng/ml) treatment produces outgrowth of long nestin-positive neurites. For analysis of the core structures, endoneuraminidase Ntreated PSA-NCAM was. Here we set up a metastatic model in nude mice by using TE671 cells, which strongly express PSA-NCAM. PSA is an oncodevelopmental antigen usually expressed in human tumors with high metastatic potential.
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