ArticleBMC cancer2019
Glioma malignancy is linked to interdependent and inverse AMOG and L1 adhesion molecule expression.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 28 citations in OpenAlex.
- Cuprotosis clusters predict prognosis and immunotherapy response in low-grade glioma.Apoptosis : an international journal on programmed cell death · 2024Article
- DeepAutoGlioma: a deep learning autoencoder-based multi-omics data integration and classification tools for glioma subtyping.BioData mining · 2023Article
- The βInternational journal of molecular sciences · 2022Article
- Artemisinin upregulates neural cell adhesion molecule L1 to attenuate neurological deficits after intracerebral hemorrhage in mice.Brain and behavior · 2022Article
- GNG5 is a novel oncogene associated with cell migration, proliferation, and poor prognosis in glioma.Cancer cell international · 2021Article
- Association Between Oral Microbiota and Human Brain Glioma Grade: A Case-Control Study.Frontiers in microbiology · 2021Article
- Ion Channels and Their Role in the Pathophysiology of Gliomas.Molecular cancer therapeutics · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
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.
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