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Glioblastoma of the brain is a malignant neoplasm characterized by aggressive development. A rare pathology among cancer patients is diagnosed one time in 1000 cases. The tumor originates in brain cells called glia. Against the background of a violation of their activity, active cell division begins, including in nearby ones – this is how the malignant process develops (Ishiuchi et al., 2007). Glioblastoma is often localized in the temporal and frontal parts of the brain, but it is sometimes diagnosed in the cerebellum, spinal cord, and brain stem. There is growing evidence that glioblastoma cells release glutamate and utilize it through autocrine or paracrine loops through Ca2+-permeable AMPA-type glutamate receptors to encourage growth and migration (Ishiuchi et al., 2007). This study has demonstrated an alternative therapy for glioblastoma by activating Akt using Ca 2+ signaling. The study used surgical specimens and cell cultures identified with glioblastoma tumors to conduct the study.
Findings
The finding of the paper shows that glutamate stimulates cell proliferation and migration. This technique can stimulate AMPA, which hinders the phosphorylation of Akt in the tumors. Additionally, the study has demonstrated that activation of Akt by Ca2+ signaling, which is mediated by the AMPA receptor, controls glioblastoma cell growth and motility (Ishiuchi et al., 2007). Proliferation and mobility were made possible by the phosphorylation of Akt at Ser-473 by Ca2+ delivered through a Ca 2+ -permeable AMPA receptor. Cell migration and proliferation that were sped up by the overexpression of the Ca2+ -permeable AMPA receptor were blocked by a dominant-negative version of Akt. In contrast, delivery of GluR2 cDNA caused Ca2+-permeable AMPA receptors to become Ca2+-impermeable receptors, which caused tumor cells to undergo apoptosis.
Relevance
This new mechanism could provide a different treatment target for glioblastoma tumors. A constitutively active version of Akt was added, and it stopped apoptosis. The therapeutic pathway can activate human glioblastoma; this gap might be bleached by the invention of this therapeutic method (Ishiuchi et al., 2007). Therefore, this new and promising therapy for glioblastoma cells will improve glioblastoma patients’ outcomes in health practice by providing an additional variety of therapy.
Reference
Ishiuchi, S., Yoshida, Y., Sugawara, K., Aihara, M., Ohtani, T., Watanabe, T.,… & Ozawa, S. (2007). Ca2+-Permeable AMPA receptors regulate the growth of human glioblastoma via Akt activation. Journal of Neuroscience, 27(30), 7987-8001. Web.
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