Overcoming therapy resistance of glioma via elucidation of the mechanisms underlying glioma stem cell maintenance

在本研究中，我们寻找了胶质母细胞瘤干细胞维持中的细胞内信号以及信号分子，并证明了PI 3 K/mTOR和MAPK在胶质母细胞瘤干细胞维持中的关键作用。值得注意的是，PI 3 K/mTOR和MAPK作用于共同的分子，即，FOXO 3转录因子，其活性通过胶质母细胞瘤干细胞中这些激酶的磷酸化而受到抑制。我们的研究结果表明FOXO 3以及这些激酶可能是干细胞靶向胶质母细胞瘤治疗的合理分子靶点。

In this study, we searched for intracellular signals as well as signaling molecules involvedin the maintenance of glioblastoma stem cells and demonstrated critical roles for PI3K/mTOR and MAPK in glioblastoma stem cell maintenance. Significantly, PI3K/mTORand MAPK acted on a common molecule, i.e., the FOXO3 transcription factor, whoseactivity was restrained through phosphorylation by these kinases in glioblastoma stemcells. Our results suggest that FOXO3 as well as these kinases could be rational moleculartargets for stem cell-targeted glioblastoma therapies.