敲除SLC39A5基因对4-NQO诱发C57BL/6小鼠食管癌模型建立的影响

目的 探索敲除SLC39A5基因对4-NQO诱导的C57BL/6小鼠食管癌模型的影响。方法 选取10只C57BL/6野生型小鼠作为阴性对照组，饮用浓度为100 μg/ml的丙二醇空白溶液；选取140只野生型小鼠与80只SLC39A5基因敲除小鼠，采用饮水法摄入诱癌剂，即浓度为100 μg/ml的4-NQO（4-nitroquinoline 1-oxide），实验时间为28周，实验结束后处死三组小鼠。结果 阴性对照组小鼠、野生型小鼠和SLC39A5基因敲除小鼠在实验结束时其存活率分别为100%、92.96%、91.25%；三组小鼠食管癌诱癌成功率分别为0、61.36%、28.77%，两实验组小鼠诱癌成功率差异有统计学意义（χ²=19.98, P<0.001）。结论 成功建立了C57BL/6小鼠及SLC39A5基因敲除小鼠的食管癌模型，同时验证了SLC39A5基因在食管癌发生发展中的促进作用。

Impact of SLC39A5 Knockout on Establishment of Esophageal Cancer Model Induced by 4-NQO in C57BL/6 Mice

Objective To explore the influences of SLC39A5 knockout on the establishment of esophageal cancer model induced by 4-nitroquinoline 1-oxide (4-NQO) in C57BL/6 mice. Methods Ten wild-type mice were treated as negative control group and drank the 1,2-propylene glycol at 100 μg/ml; 140 wild-type mice and 80 knockout genotype mice were treated as experimental groups and drank the carcinogen 4-NQO stock solution dissolved in 1,2-propylene glycol at 100μg/ml, the experimental time was 28 weeks and all three groups’ mice were sacrificed. Results The survival rates were 100%, 92.96% and 91.25% in negative group, wild-type experimental group and SLC39A5 knockout genotype experimental group, respectively; the rates of tumor formation were 0, 61.36% and 28.77%, and there was a statistical difference between the two experimental groups(χ²=19.98, P<0.001). Conclusion The esophageal cancer model in C57BL/6 mice and SLC39A5 knockout mice are established successfully and the facilitated role of SLC39A5 in the occurrence and development of esophageal cancer is verified.