Mac-1基因缺失抑制小鼠黑色素瘤肺转移的机制

Inhibitory effect of the gene deletion of Mac-1 on the lung metastasis of mouse melanoma

目的探讨Mac-1基因缺失对黑色素瘤肺转移的抑制作用。方法 Mac-1基因敲除(Mac-1-/-)小鼠配种扩群以获得实验需要的数量,取指数生长期B16细胞,分别尾静脉注射到对照组C57BL/6J小鼠和实验组Mac-1-/-小鼠体内,统计小鼠生存率及肿瘤肺转移结节数,并通过H&E观察肺组织中微转移灶。结果通过配种扩群获得了大量实验用纯合子Mac-1基因敲除小鼠(Mac-1-/-)。与对照组相比,Mac-1缺失后尾静脉注射B16细胞的小鼠存活率显著提高(P<0.001);并且大体观察Mac-1缺失后小鼠肿瘤转移肺结节数目显著减少(P<0.001),抑制率达到75%;进一步通过对肺组织包埋、切片和H&E观察发现,Mac-1缺失后小鼠肺组织中肿瘤微转移灶显著减少(P<0.001)。结论 Mac-1基因缺失能显著抑制小鼠黑色素瘤的肺转移。

Objective To study the inhibitory effect of the gene deletion of Mac-1 on the lung metastasis of melanoma. Methods Mac-1 knockout mice were mated in order to obtain the number of need. Mice melanoma cells B16 were respectively injected into the caudal vein of the control group C57BL/6J mice and the experimental group Mac-1 knockout mice. The melanoma lung metastasis nodules were examined, survival rate of mice was counted, and micro metastases in lung tissue were observed by H＆E. Results A large number of experiments with homozygous Mac-1 knockout mice （Mac-1-/-） were obtained by breeding expansion group. Compared with that of control group, the survival rate of Mac-1 knockout mice with intravenous B16 ceils was significantly increased, and the lung nodule number was significantly reduced（P〈0.001 ）, and inhibition rate reached 75%, further through the lung tissue embedding, sectioning and H＆E observation, tumor metastases of Mac-1 knockout mice was significantly reduced in the lung tissue. Conclusions The gene deletion of Mac-1 could significantly inhibite the lung metastasis of mouse melanoma.