A fundamental research for developing ubiquitin-targeted cancer therapies utilizing vesicular transport related molecules Hrs knocked-out mice.

囊泡转运相关分子HRs的缺失使c-Myc的表达减少。C-Myc过表达与癌症患者预后不良的关系已有报道。我们试图利用c-Myc的过度表达作为生物标记物来确定新的治疗靶点。我们使用由3500个可药物基因组组成的siRNA文库进行筛选，并选择酪蛋白激酶1 epsilon作为新的靶点。我们还发现酪蛋白激酶1的特异性抑制剂IC261在小鼠卵巢癌模型中具有治疗作用。

Defect of vesicle transport related molecule Hrs diminishes the expression of c-Myc. There are some reports concerning the relationship between c-Myc overexpression and poor prognosis of cancer patients. We attempted to identify new therapeutic target utilizing c-Myc overexpression as a biomarker. We used a siRNA library consists of 3500 druggable genome for a screening, and selected Casein Kinase 1 epsilon as a new target. We also showed IC261, a specific inhibitor of Casein Kinase 1 epsilon has therapeutic effects in mouse ovarian cancer model.