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PKC signaling in glioblastoma

机译:胶质母细胞瘤中的PKC信号传导

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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 largescale 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.
机译:多形胶质母细胞瘤(GBM)是最具侵略性的脑肿瘤,其特征是在细胞病理学,基因组和转录水平上的肿瘤内异质性。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中的遗传改变影响控制细胞周期进程,细胞增殖以及存活和侵袭能力的途径,这可能解释了治疗GBM患者的困难。促进神经胶质瘤细胞侵袭行为的信号传导途径之一是蛋白激酶C(PKC)途径。 PKC是根据激活域分为三类的丝氨酸/苏氨酸特异性蛋白激酶家族。由于PKC同工型所控制的作用的可变性,人们对其对GBM发展的贡献知之甚少。这篇综述旨在强调PKC同工型对神经胶质瘤细胞增殖,存活和侵袭能力的贡献。

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