Centre for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Cancer Biol Ther. 2013 Apr;14(4):287-94. doi: 10.4161/cbt.23615. Epub 2013 Jan 28.
Glioblastoma Multiforme (GBM) is the most aggressive brain tumor characterized by intratumoral heterogeneity at cytopathological, genomic and transcriptional levels. Despite the efforts to develop new therapeutic strategies the median survival of GBM patients is 12-14 months. Results from large-scale gene expression profile studies confirmed that the genetic alterations in GBM affect pathways controlling cell cycle progression, cellular proliferation and survival and invasion ability, which may explain the difficulty to treat GBM patients. One of the signaling pathways that contribute to the aggressive behavior of glioma cells is the protein kinase C (PKC) pathway. PKC is a family of serine/threonine-specific protein kinases organized into three groups according the activating domains. Due to the variability of actions controlled by PKC isoforms, its contribution to the development of GBM is poorly understood. This review intends to highlight the contribution of PKC isoforms to proliferation, survival and invasive ability of glioma cells.
胶质母细胞瘤（GBM）是最具侵袭性的脑肿瘤，其在细胞学、基因组和转录水平上具有肿瘤内异质性。尽管努力开发新的治疗策略，GBM 患者的中位生存期仍为 12-14 个月。大规模基因表达谱研究的结果证实，GBM 中的遗传改变影响了控制细胞周期进程、细胞增殖和存活以及侵袭能力的途径，这可能解释了治疗 GBM 患者的困难。导致神经胶质瘤细胞侵袭性行为的信号通路之一是蛋白激酶 C（PKC）通路。PKC 是一组丝氨酸/苏氨酸特异性蛋白激酶，根据激活结构域分为三组。由于 PKC 同工型控制的作用的可变性，其对 GBM 发展的贡献尚不清楚。本文旨在强调 PKC 同工型对神经胶质瘤细胞增殖、存活和侵袭能力的贡献。
