肿瘤干细胞被认为在肿瘤的致病中起着至关重要的作用，因此肿瘤干细胞学说认为抑制肿瘤干细胞是肿瘤治疗必不可少的过程。但是到目前为止，尚缺乏有效的化疗药物可以抑制肿瘤干细胞。申请人的预实验表明：癌症基因大有丝分裂原活化蛋白激酶1（BMK1）阻断剂XMD8-92在胶质瘤模型中可以有效地抑制干细胞表面标记CD133等的表达，同时显著降低肿瘤细胞的成球性。在此基础上，申请人提出假说- - BMK1可能在胶质瘤干细胞中起到重要作用， BMK1信号通路经由PML调节胶质瘤干细胞。为验证这一假说，我们将通过胶质肿瘤细胞系结合移植瘤小鼠模型，采用基因芯片、RT-PCR和免疫荧光等多种手段，进行癌症基因BMK1在致病机理方面的探索。本研究将从BMK1阻断剂XMD8-92在胶质瘤模型中可以有效地抑制胶质瘤干细胞这个新视点，为揭示胶质瘤干细胞的致病机制奠定基础，为胶质瘤的防治提供新思路。

Cancer stem cells play a central role in the tumorgenesis. Based on cancer stem cell hypothesis, it's essential to remove the cancer stem cell to cure cancer. However, we are still short of effective chemo targeting cancer stem cells. The data of my pilot experiment indcated that BMK1 inhibitor, XMD8-92,significantly impaired CD133 (a surface marker of cancer stem cells) and the forming of glioma neurospheres. Based on this, it is hypothsized that BMK1 plays an important role in the regulation of glioma stem cells through PML. To verify this, mouse model, gene CHIP， RT-PCR and IF (Immunofluorescence) will be carried out to evaluate the role of BMK1 in tumorgenesis. Based on the impairment of glioma stem cells by BMK1 inhibitor, this study will contribute a lot to the illumination of glioma stem cell and improvement of glioma therapy.