ArticleJournal of experimental & clinical cancer research : CR2014
Store-operated Ca(2+) entry regulates glioma cell migration and invasion via modulation of Pyk2 phosphorylation.
Article in Journal of experimental & clinical cancer research : CR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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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
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Systematic Review of Molecular Targeted Therapies for Adult-Type Diffuse Glioma: An Analysis of Clinical and Laboratory Studies.International journal of molecular sciences · 2023Pooled it
- Potential therapeutic targeting of BKMolecular oncology · 2026Review
- Plasma biomarker ORAI1 as a dual prognostic value for survival and postoperative quality of life in glioma patients.Scientific reports · 2025Article
- ORAI CaBiomolecules · 2024Review
- CRAC and SK Channels: Their Molecular Mechanisms Associated with Cancer Cell Development.Cancers · 2022Review
- Activated PyK2 and Its Associated Molecules Transduce Cellular Signaling from the Cancerous Milieu for Cancer Metastasis.International journal of molecular sciences · 2022Review
- Endoplasmic Reticulum Stress Contributed to Dipyridamole-Induced Impaired Autophagic Flux and Glioma Apoptosis.International journal of molecular sciences · 2022Article
- Review
- Receptor Tyrosine Kinase Signaling and Targeting in Glioblastoma Multiforme.International journal of molecular sciences · 2021Review
- Advances in the study of cancer metastasis and calcium signaling as potential therapeutic targets.Exploration of targeted anti-tumor therapy · 2021Review
- Mechanisms of Invasion in Glioblastoma: Extracellular Matrix, CaFrontiers in cellular neuroscience · 2021Review
- Calcium Channel Protein ORAI1 Mediates TGF-β Induced Epithelial-to-Mesenchymal Transition in Colorectal Cancer Cells.Frontiers in oncology · 2021Article
- Platelet-derived microvesicles induce calcium oscillations and promote VSMC migrationTheranostics · 2021Article
- Molecular Choreography and Structure of CaMembranes · 2020Review
- Suppression of store-operated CaCell cycle (Georgetown, Tex.) · 2020Article
- Blockage of Store-Operated CaCancers · 2020Article
- pH-Channeling in Cancer: How pH-Dependence of Cation Channels Shapes Cancer Pathophysiology.Cancers · 2020Review
- Orai1 Channel Inhibition Preserves Left Ventricular Systolic Function and Normal CaCirculation · 2020Article
- Calcium Permeable Channels in Cancer Hallmarks.Frontiers in pharmacology · 2020Review
- Roles of CRAC channel in cancer: implications for therapeutic development.Expert review of precision medicine and drug development · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe ubiquitous second messenger Ca(2+) has been demonstrated to play an important role in cancer progression. Store-operated Ca(2+) entry (SOCE) is the main Ca(2+) entry pathway regulating intracellular Ca(2+) concentration in a variety of cancer types. The present study aimed to explore the specific mechanisms of SOCE in the processes of glioma migration and invasion.
methodsThe expression of Orai1, a key component of SOCE, was examined in glioma samples and glioma cell lines by immunohistochemistry and western blot analysis. Both pharmacological intervention and RNA interference were employed to investigate the role of SOCE in glioma cell migration and invasion in vitro. The intracellular Ca(2+) was certified through Fluo-4/AM based Ca(2+) measurement. The effect of SOCE on cell viability, migration, and invasion was explored by methyl thiazolyl tetrazolium (MTT) assay, wound healing assay, transwell invasion assay. Western blot analysis and immunofluorescence assay were used to observe the changes of downstream related protein and cell morpholog.
resultsOrai1 expression was elevated in glioma tissues and several glioma cell lines compared with non-neoplastic brain tissues. Either inhibition of SOCE by a pharmacological inhibitor or Orai1 downregulation suppressed glioma cell migration and invasion. However, re-expression of Orai1 could rescue glioma cell motility. Furthermore, phosphorylation of proline-rich tyrosine kinase 2 (Pyk2) participated in the mechanisms by which SOCE regulated focal adhesion turnover and epithelial-to-mesenchymal (-like) transition in glioma cells, both of which are considered to be critical for tumor progression.
conclusionsThe SOCE-Pyk2 pathway is essential for glioma migration and invasion. The study indicates the potential value of Orai1 as a molecular target for anti-invasion therapy.
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Registered trials
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