Abstract
BackgroundGliomas account for the majority of primary human brain tumors and remain a challenging neoplasm for cure due to limited therapeutic options. Cell adhesion molecules play pivotal roles in the growth and progression of glial tumors. Roles of the adhesion molecules on glia (AMOG) and L1CAM (L1) in glioma cells have been shown to correlate with tumorigenesis: Increased expression of L1 and decreased expression of AMOG correlate with degree of malignancy.MethodsWe evaluated the interdependence in expression of these molecules by investigating the role of AMOG in vitro via modulation of L1 expression and analyzing apoptosis and cell senescence of glioma cells.ResultsImmunohistochemical staining of normal human cortical and glioma tissue microarrays demonstrated that AMOG expression was lower in human gliomas compared to normal tissue and is inversely correlated with the degree of malignancy. Moreover, reduction of AMOG expression in human glioblastoma cells elevated L1 expression, which is accompanied by decreased cell apoptosis as well as senescence.ConclusionAMOG and L1 interdependently regulate their expression levels not only in U-87 MG cells but also in U251 and SHG44 human glioma cell lines. The capacity of AMOG to reduce L1 expression suggests that methods for increasing AMOG expression may provide a therapeutic choice for the management of glial tumors with high expression of L1.
Highlights
Gliomas account for the majority of primary human brain tumors and remain a challenging neoplasm for cure due to limited therapeutic options
adhesion molecules on glia (AMOG) expression in human glioma tissue microarray A tissue microarray was subjected to immunohistochemical staining of AMOG on normal brain tissue and glioma tissues of different World Health Organization (WHO) grades
Representative immunohistochemical images of AMOG in normal human brain and different grades of human glioma tissues are shown at different magnifications (Fig. 1e)
Summary
Gliomas account for the majority of primary human brain tumors and remain a challenging neoplasm for cure due to limited therapeutic options. Roles of the adhesion molecules on glia (AMOG) and L1CAM (L1) in glioma cells have been shown to correlate with tumorigenesis: Increased expression of L1 and decreased expression of AMOG correlate with degree of malignancy. Glioma is a brain neoplasm mainly originating from glial cells It accounts for about 30% of all tumors in the human central nervous system and about 80% of the malignant ones [1, 2]. Treatment of gliomas mainly includes surgical resection, radiotherapy and chemotherapy These regimens are often not Several cell adhesion molecules have been identified to underlie the occurrence of malignancies in gliomas, including adhesion molecule on glia (AMOG) [3] and neural cell adhesion molecule L1 (L1CAM, hereafter abbreviated L1) [4, 5]. In human glioblastoma cell cultures captured from surgical specimens, enhanced levels of AMOG expression correlated positively with invasion without affecting migration or proliferation, and knock-down of AMOG expression promoted cell migration in cultures of human astrocytes [13]
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