MYCN扩增是神经母细胞瘤发生的重要基因突变，因是转录因子，迄今尚未发现恰当的靶向药物，故靶向MYCN下游调控蛋白成为治疗MYCN扩增型神经母细胞瘤的有效方法。R2数据库推测TTK/Mps1在神经母细胞瘤患者中高表达，且与患者总体生存率和无复发生存率负相关。敲低或抑制TTK致神经母细胞瘤细胞增殖减慢和细胞周期停滞。此外，CHIP-PCR实验证实MYCN通过直接靶向结合TTK启动子区并上调其表达。提示TTK/Mps1高表达有可能是神经母细胞瘤发生的风险因素，故本项目一方面通过分子细胞学实验和RNA测序技术探讨TTK/Mps1和MYCN如何相互影响，调控下游信号通路，促进肿瘤细胞增殖加快和细胞凋亡变慢等表型出现，另一方面采用动物模型挖掘抑制TTK/Mps1作为神经母细胞瘤治疗的可能性，最终建立TTK/Mps1参与神经母细胞瘤发生的完整机制，为神经母细胞瘤的靶向治疗提供又一新靶点。

MYCN amplification is an important gene mutation in neuroblastoma, but as a transcription factor, no appropriate targeted drug has been found so far. Therefore, targeting the downstream regulatory protein of MYCN has become an effective method for MYCN amplified neuroblastoma. The R2 database speculated that TTK/Mps1 was highly expressed in neuroblastoma patients and was negatively correlated with overall survival rate and relapse-free survival rate. Neuroblastoma cell proliferation slowed down and cell cycle stagnated due to knockdown or inhibition of TTK. In addition, CHIP-PCR assay confirmed that MYCN up-regulated the expression of TTK by directly targeting binding to the TTK/Mps1 promoter region. All is suggested that high TTK/Mps1 expression may be a risk factor in neuroblastoma. the project is, on the one hand, explored through the molecular cell biology experiment how TTK/Mps1 and MYCN regulate each other, which influence the downstream signaling pathways and promote tumor cell proliferation and anti-apoptosis, On the other hand, animal models were used to understand the possibility of inhibiting TTK/Mps1 as a treatment for neuroblastoma. Finally, the complete mechanism of TTK/Mps1 in the occurrence of neuroblastoma was established to provide a novel target for the neuroblastoma therapy.