AI Article Synopsis
- Cell communication is crucial for tissue development, but brain tumors like glioblastoma disrupt this process, leading to tumor growth and damage to healthy brain tissue.
- Glioblastoma produces a protein called ImpL2 that interferes with the insulin signaling in nearby neurons, causing early signs of neurodegeneration such as mitochondrial dysfunction and synapse loss.
- Restoring insulin signaling in neurons can potentially protect against neurodegeneration and could be a focus for developing new anti-tumor strategies.
Article Abstract
Cell to cell communication facilitates tissue development and physiology. Under pathological conditions, brain tumors disrupt glia-neuron communication signals that in consequence, promote tumor expansion at the expense of surrounding healthy tissue. The glioblastoma is one of the most aggressive and frequent primary brain tumors. This type of glioma expands and infiltrates into the brain, causing neuronal degeneration and neurological decay, among other symptoms. Here, we describe in a model how glioblastoma cells produce ImpL2, an antagonist of the insulin pathway, which targets neighboring neurons and causes mitochondrial disruption as well as synapse loss, both early symptoms of neurodegeneration. Furthermore, glioblastoma progression requires insulin pathway attenuation in neurons. Restoration of neuronal insulin activity is sufficient to rescue synapse loss and to delay the premature death caused by glioma. Therefore, signals from glioblastoma to neuron emerge as a potential field of study to prevent neurodegeneration and to develop anti-tumoral strategies.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7898663 | PMC |
| http://dx.doi.org/10.26508/lsa.202000693 | DOI Listing |
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