细胞转移是癌症病人死亡的最主要原因，而肿瘤干细胞的存在促进远处转移的形成。因此更好的理解肿瘤干细胞特性具有重要临床应用意义。迄今为止对结直肠癌中肿瘤干细胞产生的机制知之甚少。我们前期研究提示E2A在抑制结直肠癌干细胞产生，但其作用机制有待进一步研究。为此我们提出假说：E2A可能通过抑制β-catenin细胞核内表达影响wnt/β-catenin通路，从而抑制结直肠癌干细胞生成。为了验证这一假说，我们将通过人结直肠癌组织，细胞系和小鼠结直肠癌肝转移模型，采用Western Blot、慢病毒载体转染、干细胞球形成实验等手段，从分子，细胞及动物整体水平等多方面探讨E2A对结直肠癌细胞干细胞特性的影响，明确E2A通过wnt/β-catenin通路调节结直肠癌干细胞特性的具体机制。本研究将从E2A这个新视点为揭示结直肠癌干细胞产生机制奠定基础，为结直肠癌远处转移的治疗提供新思路。

Metastasis takes responsibility for 90 percent cancer-associated death. The generation of cancer stem cells influence the formation of metastasis. So, better understanding of cancer stem cell behavior is of clinical significance. While, the mechanisms of cancer stem cell generation are poorly understood. Our previously study illustrates E2A takes important role in colorectal cancer stem cell generation, but the mechanism of it needs more reseach to clarify. To this, we presume that E2A inhibits generation of colorectal cancer stem cell by down-regulating cell-nuclear beta-catenin expression to affect wnt/β-catenin pathway. To define the molecular mechanism of E2A regulating colorectal cancer stem cell properties, We discuss the effect of E2A on colorectal cancer stem cell properties on molecular and animal level with Western Blot, lentivirus affection, CSCs sphere formation using colorectal cancer tissues, cell lines and mouse colorectal liver metastasis model. This study will lay the foundation for revealing molecular mechanism of colorectal cancer stem cell generation and provide new way for colorectal cancer metastasis therapy from the new perspective of E2A.