ReviewNeoplasia (New York, N.Y.)2008
The sodium pump alpha1 subunit as a potential target to combat apoptosis-resistant glioblastomas.
Review in Neoplasia (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 120 citations in OpenAlex.
- Connecting the Dots: AMOG/βInternational journal of molecular sciences · 2025Review
- Update on the intriguing roles of AQP4 expression and redistribution in the progression and treatment of glioma.Annals of medicine · 2024Review
- ATP1A1 is a promising new target for melanoma treatment and can be inhibited by its physiological ligand bufalin to restore targeted therapy efficacy.Cancer cell international · 2024Article
- Markedly divergent effects of Ouabain on a Temozolomide-resistant (T98G) vs. a Temozolomide-sensitive (LN229) Glioblastoma cell line.Discover oncology · 2023Article
- Chemistry and the Potential Antiviral, Anticancer, and Anti-Inflammatory Activities of Cardiotonic Steroids Derived from Toads.Molecules (Basel, Switzerland) · 2022Review
- Homophilic ATP1A1 binding induces activin A secretion to promote EMT of tumor cells and myofibroblast activation.Nature communications · 2022Article
- Therapeutic Applications of Physalins: Powerful Natural Weapons.Frontiers in pharmacology · 2022Review
- Tumor Tissue Oxidative Stress Changes and Na, K-ATPase Evaluation in Head and Neck Squamous Cell Carcinoma.The Journal of membrane biology · 2021Article
- Preeclampsia: Cardiotonic Steroids, Fibrosis, Fli1 and Hint to Carcinogenesis.International journal of molecular sciences · 2021Review
- Membrane Transporters and Channels in Melanoma.Reviews of physiology, biochemistry and pharmacology · 2021Review
- Spider venom components decrease glioblastoma cell migration and invasion through RhoA-ROCK and NaCancer cell international · 2020Article
- ATP1A1 Integrates AKT and ERK Signaling via Potential Interaction With Src to Promote Growth and Survival in Glioma Stem Cells.Frontiers in oncology · 2019Article
- Sodium chloride (NaCl) potentiates digoxin-induced anti-tumor activity in small cell lung cancer.Cancer biology & therapy · 2019Article
- Targeting β2 subunit of NaAmerican journal of cancer research · 2019Article
- Molecular Markers of Therapy-Resistant Glioblastoma and Potential Strategy to Combat Resistance.International journal of molecular sciences · 2018Review
- The predictive potential of hyponatremia for glioblastoma patient survival.Journal of neuro-oncology · 2018Article
- Marinobufagenin inhibits glioma growth through sodium pump α1 subunit and ERK signaling-mediated mitochondrial apoptotic pathway.Cancer medicine · 2018Article
- Cardiac Glycoside Glucoevatromonoside Induces Cancer Type-Specific Cell Death.Frontiers in pharmacology · 2018Article
- Anticancer and Immunogenic Properties of Cardiac Glycosides.Molecules (Basel, Switzerland) · 2017Review
- The Na, K-ATPase β-Subunit Isoforms Expression in Glioblastoma Multiforme: Moonlighting Roles.International journal of molecular sciences · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo review the involvement of the ion transporter Na+/K+-ATPase (NaK) in the migration and proliferation of glioma cells. Preliminary studies indicate that NaK alpha1 subunits seem to be upregulated in a proportion of glioblastomas but not in normal brain tissues.
designThe present review focuses on (1) the natural resistance of migrating malignant glioma cells to apoptosis, (2) autophagic cell death as an alternative to combat malignant gliomas, (3) the fact that reducing the levels of malignant glioma cell motility can restore proapoptotic drug sensitivity,and (4) on the observation that inhibiting the NaK activity reduces both glioma cell proliferation and migration.
resultsThe natural ligands of the NaK are the cardiotonic steroids. A hemisynthetic derivative of 2"-oxovoruscharin (UNBS1450), a novel cardenolide, displays unique structural features, making its binding affinity to NaK alpha subunits (including alpha1) 10 to 100 times higher than that of other cardenolides. UNBS1450 markedly decreases intracellular ATP concentration in glioma cells, disorganizes the actin cytoskeleton, and leads to autophagic cell death in NaK alpha1 over-expressing glioma cells.
conclusionsGlioblastoma patients who do not respond to chemotherapy and whose tumors over-express NaK alpha1 subunits could benefit from a treatment using ligands with marked binding affinity for the NaK alpha1 subunit.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.