Pridham Kevin J, Varghese Robin T, Sheng Zhi
Virginia Tech Carilion Research Institute, Virginia Tech, Roanoke, VA, United States.
Graduate Program in Translational Biology, Medicine, and Health, Virginia Tech, Blacksburg, VA, United States.
Front Oncol. 2017 Dec 15;7:312. doi: 10.3389/fonc.2017.00312. eCollection 2017.
Phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) plays a critical role in the pathogenesis of cancer including glioblastoma, the most common and aggressive form of brain cancer. Targeting the PI3K pathway to treat glioblastoma has been tested in the clinic with modest effect. In light of the recent finding that PI3K catalytic subunits (PIK3CA/p110α, PIK3CB/p110β, PIK3CD/p110δ, and PIK3CG/p110γ) are not functionally redundant, it is imperative to determine whether these subunits play divergent roles in glioblastoma and whether selectively targeting PI3K catalytic subunits represents a novel and effective strategy to tackle PI3K signaling. This article summarizes recent advances in understanding the role of PI3K catalytic subunits in glioblastoma and discusses the possibility of selective blockade of one PI3K catalytic subunit as a treatment option for glioblastoma.
磷脂酰肌醇-4,5-二磷酸3-激酶（PI3K）在包括胶质母细胞瘤在内的癌症发病机制中起关键作用，胶质母细胞瘤是最常见且侵袭性最强的脑癌形式。针对PI3K通路治疗胶质母细胞瘤已在临床上进行了测试，但效果一般。鉴于最近的发现，即PI3K催化亚基（PIK3CA/p110α、PIK3CB/p110β、PIK3CD/p110δ和PIK3CG/p110γ）在功能上并非冗余，因此必须确定这些亚基在胶质母细胞瘤中是否发挥不同作用，以及选择性靶向PI3K催化亚基是否代表一种应对PI3K信号传导的新颖且有效的策略。本文总结了在理解PI3K催化亚基在胶质母细胞瘤中的作用方面的最新进展，并讨论了选择性阻断一种PI3K催化亚基作为胶质母细胞瘤治疗选择的可能性。
