摘要
目的观察B7-H3对Lewis肺癌(LLC)细胞生长的影响并探讨其作用机制。方法采用40只C57BL/6小鼠,右腋下接种Lewis肺癌细胞悬液,建立皮下种植瘤模型,随机分为4组,在瘤体附近皮下围绕瘤体分别注射多西他赛、B7-H3及多西他赛+B7-H3,以注射空质粒作为对照。注射后第1、3、7、14天测量肿瘤的大小,计算肿瘤的体积;采用免疫组织化学及Western blot检测瘤组织中B7-H3的表达;采用ELISA检测小鼠血清IL-12的水平。结果多西他赛和B7-H3均能分别抑制肿瘤的生长,两者联合则抑制作用增强,多西他赛组、B7-H3组及多西他赛+B7-H3组的抑瘤率分别为32.98%、28.59%和45.95%,上述处理后肿瘤细胞凋亡率均比对照组明显提高(P<0.01);B7-H3组及多西他赛+B7-H3组肿瘤组织中B7-H3的表达下调,但差异无统计学意义(P>0.05);小鼠血清中IL-12的表达在B7-H3组及多西他赛+B7-H3组均较对照组水平升高(P<0.05)。结论 B7-H3能抑制小鼠Lewis肺癌细胞的生长,其机制可能与通过IL-12诱导激活细胞毒性T细胞而产生抗肿瘤免疫应答有关。
Objective To study the inhibitive effect of B7-H3 on the growth of Lewis lung carcinomas （LLC） cell. Methods Forty C57BL/6 mice were subcutaneously inoculated with LLC ceils suspension （1×107/ml） in the right armpit. The tumor-bearing mice were randomly divided into four groups： empty plasmid （as control）, docetaxel,B7-H3 and docetaxel ＋ BT-H3 were injected subcutaneously around the tumor. Tumor sizes were valued at the first, third, seventh and fourteenth day after injection. B7-H3 ex- pression was detected by immunohistochemistry and Western blot. The level of serum IL-12 was detected by ELISA. Results Tumor was inhibited by doeetaxel and B7 H3. The inhibitory rates in the groups of docetaxel, B7-H3 and doeetaxel ＋ t37-H3 were 32.98%,28.59% and 45.95 G, respectively. The apoptosis rate of tumor cells after treatment was significantly increased （P〈0. 01）. BT-H3 expression in tumor tis- sue decreased in the groups of B7-H3 and docetaxel ＋ BT-H3, although the difference was not significant （P〉0.05）. The level of serum IL-12 increased in the groups of B7-H3 and doeetaxel ＋ B7-H3 than that in control group （P〈0.05）. Conclusion B7-H3 can inhibit the growth of murine Lewis lung cancer cell, and promote cytotoxic T cells induced by IL-12 leading to anti-tumor immune response.
出处
《肿瘤防治研究》
CAS
CSCD
北大核心
2012年第4期376-380,共5页
Cancer Research on Prevention and Treatment
基金
苏州市社会发展基金资助项目(SZD0882)
