Cellular Signalling Laboratory, Department of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna, 40126, Bologna, Italy.
Functional and Molecular Neuroimaging Unit, IRCCS Istituto Delle Scienze Neurologiche Di Bologna, 40139, Bologna, Italy.
Cell Mol Life Sci. 2022 Mar 18;79(4):195. doi: 10.1007/s00018-022-04198-1.
Glioblastoma represents the most lethal brain tumor in adults. Several studies have shown the key role of phospholipase C β1 (PLCβ1) in the regulation of many mechanisms within the central nervous system suggesting PLCβ1 as a novel signature gene in the molecular classification of high-grade gliomas. This study aims to determine the pathological impact of PLCβ1 in glioblastoma, confirming that PLCβ1 gene expression correlates with glioma's grade, and it is lower in 50 glioblastoma samples compared to 20 healthy individuals. PLCβ1 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 β-catenin, ERK1/2 and Stat3 pathways, are also affected by PLCβ1 silencing. These data suggest a potential role of PLCβ1 in maintaining a normal or less aggressive glioma phenotype.
胶质母细胞瘤是成人中最致命的脑肿瘤。多项研究表明，磷脂酶 Cβ1（PLCβ1）在中枢神经系统内多种机制的调节中起着关键作用，提示 PLCβ1 可作为高级别神经胶质瘤分子分类的新型特征基因。本研究旨在确定 PLCβ1 在胶质母细胞瘤中的病理影响，证实 PLCβ1 基因表达与胶质瘤的分级相关，与 20 名健康个体相比，50 例胶质母细胞瘤样本中的 PLCβ1 表达水平较低。PLCβ1 在细胞系和原代星形胶质细胞中的沉默导致细胞迁移和侵袭增加，间充质转录因子和标志物（如 Slug 和 N-Cadherin 以及金属蛋白酶）的表达增加。PLCβ1 沉默还会影响细胞增殖，通过增加 Ki-67 表达，以及主要的生存途径，如β-catenin、ERK1/2 和 Stat3 途径。这些数据表明 PLCβ1 在维持正常或侵袭性较低的胶质母细胞瘤表型方面可能发挥作用。
