目的：探讨混合谱系白血病5（MLL5）基因在小鼠结肠癌CT26细胞移植瘤生长中的作用及其分子机制。方法：利用 CRISPR/Cas9技术构建MLL5基因缺失、MLL5和DDX58双基因缺失的结肠癌CT26细胞模型，用Sanger测序和WB法验证敲除 效果。将基因敲除的CT26细胞接种到野生型BALB/c小鼠和免疫缺陷型NSG小鼠皮下，构建基因缺失结肠癌CT26细胞移植瘤 小鼠模型，并观察移植瘤的生长及荷瘤小鼠的总生存期（OS）。结果：在野生型小鼠中，MLL5基因缺失的CT26细胞移植瘤生长 速度显著性低于野生型癌细胞移植瘤，并延长荷瘤小鼠的OS（P

Objective: To investigate the effect of mixed lineage leukemia 5 (MLL5) gene on growth of colon cancer CT26 cell transplanted tumors in mice and its molecular mechanism. Methods: The colon cancer CT26 cell model with MLL5 gene deletion or double deletion of MLL5 and DDX58 (encoding RIG-1 gene) was constructed using CRISPR/Cas9 technology, and the knock-out efficiency was verified using Sanger sequencing and WB. Then, the constructed CT26 cells were inoculated into the scapular subcutaneous tissues of wild BALB/c mice and immunodeficient mice (NSG) to establish the gene-deficient CT26 cell transplanted tumor model. The tumor growth and the overall survival (OS) of tumor-bearing mice were observed. Results: In wild BALB/c mice, MLL5 gene depletion significantly slowed the tumor growth down and prolonged the OS of mice as compared with the mice transplanted with CT26 cells with normal MIL5 expression (P

上海市卫生和计划生育委员会青年项目（No. 20194Y0462）