Amazing stuff! Cancer is history (soon)!
"... Many gliomas arise from, or contain cells that closely resemble, oligodendrocyte precursor cells (OPCs), which are immature support cells in the brain. These OPC-like cells are a major part of tumors such as glioblastoma (GBM) and H3K27M-altered diffuse midline glioma (DMG). What makes this especially interesting is how closely glioma cells mirror healthy OPCs, sharing many of the same biological behaviors. ..."
From the abstract:
"Glioma pathophysiology is robustly regulated by interactions with neurons. Key to these interactions is the role of neuroligin-3 (NLGN3), a synaptic adhesion molecule shed in response to neuronal activity that functions as a paracrine factor crucial for glioma growth.
Here we elucidate the mechanistic pathway whereby shed NLGN3 interacts with glioma and their normal glial counterparts.
NLGN3 binds to chondroitin sulfate proteoglycan 4 (CSPG4, also known as NG2) on both glioma and healthy oligodendrocyte precursor cells (OPCs), facilitating CSPG4 shedding by ADAM10.
NLGN3–CSPG4 interactions alter membrane tension, thereby activating mechanotransducers, primarily PIEZO1, leading to membrane depolarization and subsequent ADAM10-mediated CSPG4 shedding.
The NLGN3–CSPG4–PIEZO1 pathway maintains OPCs in an undifferentiated, stem-like state and promotes glioma proliferation, underscoring its dual roles in healthy and malignant contexts."
It appears there is no original news release about this research by any of the involved institutions.
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