ArticleNeuro-oncology2013
Na⁺/K⁺-ATPase β2-subunit (AMOG) expression abrogates invasion of glioblastoma-derived brain tumor-initiating cells.
Article in Neuro-oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Monitoring glioblastoma extracellular vesicle evolution using a nanodiagnostic platform to detect glioma stem cells driving recurrent disease.Science advances · 2026Article
- Connecting the Dots: AMOG/βInternational journal of molecular sciences · 2025Review
- Overexpression of ATP1B2 promotes cancer cell migration and inhibits apoptosis in patients with esophageal squamous cell carcinoma.Oncology reports · 2025Article
- In silico studies provide new structural insights into trans-dimerization of β1 and β2 subunits of the Na+, K+-ATPase.PloS one · 2025Article
- The study of an anoikis-related signature to predict glioma prognosis and immune infiltration.Journal of cancer research and clinical oncology · 2023Article
- The Big Picture of Glioblastoma Malignancy: A Meta-Analysis of Glioblastoma Proteomics to Identify Altered Biological Pathways.ACS omega · 2021Article
- Clinical significance of P-class pumps in cancer.Oncology letters · 2021Review
- Fibrinogen in the glioblastoma microenvironment contributes to the invasiveness of brain tumor-initiating cells.Brain pathology (Zurich, Switzerland) · 2021Article
- Spider venom components decrease glioblastoma cell migration and invasion through RhoA-ROCK and NaCancer cell international · 2020Article
- Ion Channels and Their Role in the Pathophysiology of Gliomas.Molecular cancer therapeutics · 2020Review
- Kernel Differential Subgraph Analysis to Reveal the Key Period Affecting Glioblastoma.Biomolecules · 2020Article
- TET1 regulates DNA repair in human glial cells.Toxicology and applied pharmacology · 2019Article
- Glioma malignancy is linked to interdependent and inverse AMOG and L1 adhesion molecule expression.BMC cancer · 2019Article
- Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (NaInternational journal of environmental research and public health · 2019Review
- Targeting β2 subunit of NaAmerican journal of cancer research · 2019Article
- Glycogenolysis in Acquired Glioma Resistance to Temozolomide: A Role for the [CaFrontiers in pharmacology · 2018Article
- The Na, K-ATPase β-Subunit Isoforms Expression in Glioblastoma Multiforme: Moonlighting Roles.International journal of molecular sciences · 2017Article
- P2C-Type ATPases and Their Regulation.Molecular neurobiology · 2016Review
- Na,K-ATPase β1-subunit is a target of sonic hedgehog signaling and enhances medulloblastoma tumorigenicity.Molecular cancer · 2015Article
- Disseminated Medulloblastoma in a Child with Germline BRCA2 6174delT Mutation and without Fanconi Anemia.Frontiers in oncology · 2015Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMechanisms of glioma invasion remain to be fully elucidated. Glioma cells within glioblastoma multiforme (GBM) range from well-differentiated tumor cells to less-differentiated brain tumor-initiating cells (BTICs). The β2-subunit of Na(+)/K(+)-ATPase, called the adhesion molecule on glia (AMOG), is highly expressed in normal glia but is thought to be universally downregulated in GBM. To test our hypothesis that expression of AMOG is heterogeneous in GBM and confers a less invasive phenotype, we compared it between BTICs and differentiated cells from patient-matched GBM and then tested GBM invasion in vitro after AMOG overexpression.
methodsImmunohistochemistry, immunoblotting, and real-time PCR were used to characterize AMOG protein and mRNA expression in tumor samples, BTICs, and differentiated cells. Matrigel invasion assay, scratch assay, and direct cell counting were used for testing in vitro invasion, migration, and proliferation, respectively.
resultsWhile AMOG expression is heterogeneous in astrocytomas of grades II-IV, it is lost in most GBM. BTICs express higher levels of AMOG mRNA and protein compared with patient-matched differentiated tumor cells. Overexpression of AMOG decreased GBM cell and BTIC invasion without affecting migration or proliferation. Knockdown of AMOG expression in normal human astrocytes increased invasion.
conclusionsAMOG expression inhibits GBM invasion. Its downregulation increases invasion in glial cells and may also represent an important step in BTIC differentiation. These data provide compelling evidence implicating the role of AMOG in glioma invasion and provide impetus for further investigation.
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