Impact of phospholipase C β1 in glioblastoma: a study on the main mechanisms of tumor aggressiveness

Glioblastoma represents the most lethal brain tumor in adults. Several studies have shown the key role of phospholipase C beta 1 (PLC beta 1) in the regulation of many mechanisms within the central nervous system suggesting PLC beta 1 as a novel signature gene in the molecular classification of high-grade gliomas. This study aims to determine the pathological impact of PLC beta 1 in glioblastoma, confirming that PLC beta 1 gene expression correlates with glioma's grade, and it is lower in 50 glioblastoma samples compared to 20 healthy individuals. PLC beta 1 silencing in cell lines and primary astrocytes, leads to increased cell migration and invasion, with the increment of mesenchymal transcription factors and markers, as Slug and N-Cadherin and metalloproteinases. Cell proliferation, through increased Ki-67 expression, and the main survival pathways, as beta-catenin, ERK1/2 and Stat3 pathways, are also affected by PLC beta 1 silencing. These data suggest a potential role of PLC beta 1 in maintaining a normal or less aggressive glioma phenotype.

Automated summary

This study aims to determine the pathological impact of PLC beta 1 in glioblastoma. The results showed that PLC beta 1 gene expression correlates with glioma's grade, and silencing PLC beta 1 leads to increased cell migration, invasion, and proliferation in glioblastoma cells.