ArticlePloS one2009
Isoform-specific contributions of alpha-actinin to glioma cell mechanobiology.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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.
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Who cites it
54 citing papers in PubMed, 96 citations in OpenAlex.
- Mechanotransduction in glioma stem cell fate determination: from niche mechanics to therapeutic vulnerability and state plasticity.Frontiers in cell and developmental biology · 2026Review
- Mechanical observables of cancer invasion: actin, adhesion, and metastatic plasticity.Frontiers in cell and developmental biology · 2026Review
- A Genetic Perspective to Reveal the Impact of Mitochondrial Dysfunction-related Genes on Diabetic Kidney Disease: A Multi-omics Study.Current medicinal chemistry · 2026Article
- Identification of key genes involved in collagen hydrogel-induced chondrogenic differentiation of mesenchymal stem cells through transcriptome analysis: the role of m6A modification.Journal of materials science. Materials in medicine · 2024Article
- Automatic Text-Mining Approach to Identify Molecular Target Candidates Associated with Metabolic Processes for Myotonic Dystrophy Type 1.International journal of environmental research and public health · 2023Article
- Glioblastoma cell motility depends on enhanced oxidative stress coupled with mobilization of a sulfurtransferase.Cell death & disease · 2022Article
- miR-218 affects the ECM composition and cell biomechanical properties of glioblastoma cells.Journal of cellular and molecular medicine · 2022Article
- A computational modeling of invadopodia protrusion into an extracellular matrix fiber network.Scientific reports · 2022Article
- Novel Brain-Stiffness-Mimicking Matrix Gel Enables Comprehensive Invasion Analysis of 3D Cultured GBM Cells.Frontiers in molecular biosciences · 2022Article
- Mechanotransduction: Exploring New Therapeutic Avenues in Central Nervous System Pathology.Frontiers in neuroscience · 2022Review
- ECM Mechanoregulation in Malignant Pleural Mesothelioma.Frontiers in bioengineering and biotechnology · 2022Article
- Review
- Article
- High Expression Levels ofJournal of Cancer · 2019Article
- Role of Microenvironment in Glioma Invasion: What We Learned from In Vitro Models.International journal of molecular sciences · 2018Review
- Biophysical subsets of embryonic stem cells display distinct phenotypic and morphological signatures.PloS one · 2018Article
- Molecular and Genetic Determinants of Glioma Cell Invasion.International journal of molecular sciences · 2017Review
- Influence of Inherent Mechanophenotype on Competitive Cellular Adherence.Annals of biomedical engineering · 2017Article
- Mitochondrial DNA 3243A>G heteroplasmy is associated with changes in cytoskeletal protein expression and cell mechanics.Journal of the Royal Society, Interface · 2017Article
- Comparison of viscoelastic properties of cancer and normal thyroid cells on different stiffness substrates.European biophysics journal : EBJ · 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
3 authors at 1 institution in 2 countries.
Funding
Abstract
Glioblastoma Multiforme (GBM) is a malignant astrocytic tumor associated with low survival rates because of aggressive infiltration of tumor cells into the brain parenchyma. Expression of the actin binding protein alpha-actinin has been strongly correlated with the invasive phenotype of GBM in vivo. To probe the cellular basis of this correlation, we have suppressed expression of the nonmuscle isoforms alpha-actinin-1 and alpha-actinin-4 and examined the contribution of each isoform to the structure, mechanics, and motility of human glioma tumor cells in culture. While subcellular localization of each isoform is distinct, suppression of either isoform yields a phenotype that includes dramatically reduced motility, compensatory upregulation and redistribution of vinculin, reduced cortical elasticity, and reduced ability to adapt to changes in the elasticity of the extracellular matrix (ECM). Mechanistic studies reveal a relationship between alpha-actinin and non-muscle myosin II in which depletion of either alpha-actinin isoform reduces myosin expression and maximal cell-ECM tractional forces. Our results demonstrate that both alpha-actinin-1 and alpha-actinin-4 make critical and distinct contributions to cytoskeletal organization, rigidity-sensing, and motility of glioma cells, thereby yielding mechanistic insight into the observed correlation between alpha-actinin expression and GBM invasiveness in vivo.
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What OpenQuestion holds
Registered trials
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.