Altered expression of β-catenin/E-cadherin in meningiomas

Aims : Meningiomas are generally slow‐growing benign tumours representing approximately 20% of all primary intracranial tumours. The hallmark of tumorigenesis of meningiomas is the loss of chromosome 22, including loss of heterozygosity of the neurofibromatosis type 2 (NF2) gene. The NF2 encoded protein merlin appears to function as a tumour suppressor gene by controlling cadherin‐mediated cell–cell adhesion. The E‐cadherin cell adhesion system includes β‐catenin that indirectly connects cadherin to actin filaments. The aim of this study was to analyse the expression and the subcellular location of E‐cadherin and β‐catenin in human meningiomas, including meningiomas of different histomorphological subtypes and different World Health Organization (WHO) grades. Methods and results : Immunohistochemical analysis revealed lack of E‐cadherin expression at the cell membrane in 34% of meningiomas independent of their WHO grade. Loss of membranous β‐catenin occurred in 79% of meningiomas. An intense perinuclear granular immunoreactivity of β‐catenin without nuclear location was detected in the majority of meningiomas. Both immunofluorescence and Western blot analysis of fractionated meningioma cells located β‐catenin mostly on the Golgi apparatus and ER/Golgi intermediate compartment (ERGIC). Cytogenetic analysis of meningiomas showed no correlation between NF2 loss and the loss of the proper location of β‐catenin. Conclusions : The lack of membranous β‐catenin and/or membranous E‐cadherin in meningiomas may indicate an altered interaction between meningioma cells independent of loss of NF2 and independent of the tumour grade.