Iwanami Akio, Cloughesy Timothy F, Mischel Paul S
Department of Pathology and Laboratory Medicine, the Henry Singleton Brain Tumor Program at the David Geffen University of California at Los Angeles School of Medicine, Los Angeles, California 90095, USA.
Genes Dev. 2009 Aug 1;23(15):1699-704. doi: 10.1101/gad.1832909.
The phosphatidyl-inosital-3 kinase (PI3K) signaling pathway is critical for normal brain development and function and is commonly hyperactivated in brain cancer. The PTEN (phosphatase and tensin homolog deleted on chromosome 10) tumor suppressor protein and phosphate-depended kinase 1 (PDK-1) are critical regulators of this pathway. In the July 15, 2009, issue of Genes & Development, Chalhoub and colleagues (pp. 1619-1624) demonstrate PDK1-dependent and PDK1-independent effects of conditional PTEN deletion in the brain, and they identify cell type-specific differences in feedback regulation of the PI3K pathway. These studies provide important insights as to how neurons and glia may differentially regulate PI3K signaling, yielding intriguing clues about targeting PTEN-deficient brain cancers.
磷脂酰肌醇-3激酶（PI3K）信号通路对正常脑发育和功能至关重要，且在脑癌中通常过度激活。PTEN（第10号染色体缺失的磷酸酶及张力蛋白同源物）肿瘤抑制蛋白和磷酸依赖性激酶1（PDK-1）是该通路的关键调节因子。在2009年7月15日的《基因与发育》杂志上，Chalhoub及其同事（第1619 - 1624页）证明了大脑中条件性PTEN缺失的PDK1依赖性和非PDK1依赖性效应，并确定了PI3K通路反馈调节中的细胞类型特异性差异。这些研究为神经元和神经胶质细胞如何差异调节PI3K信号传导提供了重要见解，为靶向PTEN缺陷型脑癌提供了有趣的线索。
