ArticleBMC cancer2006
In vivo glioblastoma growth is reduced by apyrase activity in a rat glioma model.
Article in BMC cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 95 citations in OpenAlex.
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- Enhanced Microglia Activation and Glioma Tumor Progression by Inflammagen Priming in Mice with Tumor Necrosis Factor Receptor Type 2 Deficiency.Life (Basel, Switzerland) · 2021Article
- Ectonucleotidases in Inflammation, Immunity, and Cancer.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- Hydrolysates from bee pollen could induced apoptosis in human bronchogenic carcinoma cells (ChaGo-K-1).Journal of food science and technology · 2021Article
- Role of Purinome, A Complex Signaling System, In Glioblastoma Aggressiveness.Frontiers in pharmacology · 2021Article
- Simultaneous impact of atorvastatin and mesenchymal stem cells for glioblastoma multiform suppression in rat glioblastoma multiform model.Molecular biology reports · 2020Article
- Glioblastoma hijacks microglial gene expression to support tumor growth.Journal of neuroinflammation · 2020Article
- Role of the P2X7 receptor inOncotarget · 2019Article
- CD73 Downregulation Decreases In Vitro and In Vivo Glioblastoma Growth.Molecular neurobiology · 2019Article
- Drug resistance and combating drug resistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2019Article
- Extracellular ATP is Differentially Metabolized on Papillary Thyroid Carcinoma Cells Surface in Comparison to Normal Cells.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2018Article
- P2Y14 receptor activation decreases interleukin-6 production and glioma GL261 cell proliferation in microglial transwell cultures.Journal of neuro-oncology · 2018Article
- Article
- An autophagy-driven pathway of ATP secretion supports the aggressive phenotype of BRAFAutophagy · 2017Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundATP is an important signalling molecule in the peripheral and central nervous system. Both glioma growth and tumor resection induces cell death, thus liberating nucleotides to the extracellular medium. Nucleotides are hydrolyzed very slowly by gliomas when compared with astrocytes and induce neuronal cell death and glioma proliferation. The objective of the present study was to test the involvement of extracellular ATP in glioblastoma growth in a rat glioma model.
methodsTo deplete the extracellular ATP, the enzyme apyrase was tested on the treatment of gliomas implanted in the rats CNS. One million glioma C6 cells in 3 microliters of DMEM/FCS were injected in the right striata of male Wistar rats, 250-270 g. After 20 days, the rats were decapitated and the brain sectioning and stained with hematoxylin and eosine. We performed immunohistochemical experiments with Ki67, CD31 and VEGF. Total RNA was isolated from cultured glioma C6 cells and the cDNA was analyzed by Real Time-PCR with primers for the NTPDase family.
resultsC6 glioma cells effectively have a low expression of all NTPDases investigated, in comparison with normal astrocytes. The implanted glioma co-injected with apyrase had a significant reduction in the tumor size (p < 0.05) when compared with the rats injected only with gliomas or with gliomas plus inactivated apyrase. According to the pathological analysis, the malignant gliomas induced by C6 injection and co-injected with apyrase presented a significant reduction in the mitotic index and other histological characteristics that indicate a less invasive/proliferative tumor. Reduction of proliferation induced by apyrase co-injection was confirmed by counting the percentage of Ki67 positive glioma cell nuclei. According to counts with CD31, vessel density and neoformation was higher in the C6 group 20 days after implantation. Confirming this observation, rats treated with apyrase presented less VEGF staining in comparison to the control group.
conclusionThese results indicate that the participation of extracellular ATP and the ecto-nucleotidases may be associated with the development of this type of brain tumor in an in vivo glioma model.
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