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Cell Journal، جلد ۲۱، شماره ۱، صفحات ۶۲-۶۹
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عنوان انگلیسی Evaluation of Tumor Regulatory Genes and Apoptotic Pathways in The Cytotoxic Effect of Cytochalasin H on Malignant Human Glioma Cell Line (U87MG)
چکیده انگلیسی مقاله Objective: Glioblastoma (GBM) is the most common type of malignant brain tumor. Owing to an extensive number of tissues surrounding the brain and the aggressive nature of its attack, the treatment of glioblastoma is very difficult. Therefore, it is important to investigate new therapeutic approaches for this disease. Materials and methods: In the present experimental study, we have examined cytochalasin H cytotoxicity activities as a new therapeutic agent on U87MG cells in vitro for the first time. The cells were cultured and treated with 10-5-10-9 M of cytochalasin H for 24, 48 and 72 hours. The assessment of cell viability was carried out by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide assay at 578 nm. The data are the average of three independent tests. The expression chang¬es of PLAU and PCDH10 were then quantified by Real-Time PCR .The fluorometric of caspases 3, 8, and 9 activities were carried out. The morphology changes in the U87MG cells were observed by fluorescence microscope. Results: The MTT assay showed that cytochalasin H (10-5M) inhibited the U87MG cancer cells proliferation for 48 hours. The Real-time PCR showed that the PLAU expression was significantly decreased in comparison with that in the control (p< 0.05). The expression of PCDH10 also showed a significant increase when compared with the control (p< 0.05). Fluorescence microscopy indicated morphological changes due to apoptosis in U87MG cancer cells after treatment with cytochalasin H (10-5M, 48 hours). The fluorometric evaluation of caspase 3, 8, and 9 activities showed that there were no significant differences amongst the caspases and the control group. Conclusion: This research project program shows the caspase-independent pathways of the programmed cell death in the U87MG cancer cell line under cytochalasin H treatment. Further studies are needed to explore the exact mechanism.
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نویسندگان مقاله | Samane Heidarzade


| Gholamreza Motalleb


| Mohammad Jalil Zorriehzahra


نشانی اینترنتی http://celljournal.org/journal/article/abstract/5948
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