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Introduction: Wnt pathway serves different cell functions in gliomas, among which cell proliferation and malignancy. In cell lines it appears as instrumental to stemness and to regulate fate and differentiation. Materials and methods: Wnt3a, TCF-4, GSK3β, and β-catenin have been studied by immunohistochemistry on paraffin sections of 20 gliomas, by molecular genetics procedures in fresh tissue extracts and by immunofluorescence in 5 glioblastoma cell lines. Results: Wnt3a is not reliably detected by immunohistochemistry, whereas GSK-3β is constantly expressed in cytoplasms and on the cell membranes. Both were not expressed in low-grade gliomas. β-catenin was expressed in the cytoplasms and cell membranes. TCF-4 was positive in the nuclei of all gliomas, and in glioblastomas it reached a high intensity expression in nuclei that paralleled those positive for Ki-67/MIB.1. Very importantly, nuclear translocation of β-catenin was never observed immunohistochemically, but with fractionated western blotting. Conclusion: Wnt3a pathway is associated with malignancy in gliomas and, in particular, TCF-4 expression with Ki-67/MIB.1 distribution. β-catenin is ubiquitary, but no nuclear translocation was observed immunohistochemically. However, it translocates to activate TCF-4. The correlation of TCF-4 and Ki-67/MIB.1 labelling index needs further investigations.