IL-6/p-AKT/p-STAT3信号通路在PRL-3促进结肠癌细胞增殖、迁移中的机制研究  

Phosphatase of regenerating liver-3 promotes colon cancer cells proliferation and migration depends on paracrine IL-6 / p-AKT / p-STAT3 signaling

作　　者：来伟[1] 施景龙 林显敢[3] 许鹤洋[1] 蓝球生 褚忠华[1] 

机构地区：[1]广州中山大学孙逸仙纪念医院胃肠外科,510120 [2]广州南沙区第一人民医院普外科,511400 [3]广州中山大学孙逸仙纪念医院肿瘤科,510120

出　　处：《岭南现代临床外科》2016年第5期517-520,共4页Lingnan Modern Clinics in Surgery

基　　金：广东省科技计划项目(2013B051000025;2015A050502021);广东省医学科研基金(B2014133)

摘　　要：目的探讨细胞因子白介素(IL)-6信号通路在促进结肠癌细胞增殖、迁移中的作用机制。方法酶联免疫吸附试验ELISA检测空白组Lo Vo-Control(Lo Vo-C)结肠癌细胞和稳定表达PRL-3的实验组Lo Vo-PRL-3(Lo Vo-P)结肠癌细胞分别与肿瘤相关性巨噬细胞共培养后IL-6蛋白水平表达差异;Western blot检测IL-6、p-AKT、p-STAT3蛋白水平表达,划痕实验和增殖实验MTS检不同浓度(1、10、100 NG/ML)IL-6对结肠癌细胞侵袭及增值能力的影响。结果ELISA实验检测IL-6蛋白平,TAM/Lo Vo-P(102±5)PG/ML,TAM/Lo Vo-C为(56±3)PG/ML;划痕实验与MTS结果均提示共培养后Lo Vo-P增殖、侵袭能力比Lo Vo-C强;Western blot检测共培养后的结肠癌细胞Lo Vo-P、Lo Vo-C蛋白表达差异,p-AKT、p-STAT3表达Lo Vo-P明显高于Lo Vo-C,不同浓度的IL-6(1、10、100 NG/ML)作用Lo Vo-P后其增殖与侵袭能力逐渐增高,且p-AKT与p-STAT3蛋白水平逐渐增高。结论 PRL-3能诱导肿瘤相关性巨噬细胞分泌IL-6,通过IL-6上调p-AKT和p-STAT3促进结肠癌细胞增殖、侵袭。Objective To investigate mechanism of cytokines of interleukin （IL）-6 in promoting the colorectal cancer cells proliferation and migration. Methods We used ELISA to detect the level of IL-6 in culture medium of TAMs after co-culture with control group：LoVo-PRL-3 （LoVo-P） andexperimental group：LoVo-Control （LoVo-C）. Western blot was used to detect the proteins of p-AKT and p-STAT3. The migration and proliferation were measure by wound healing and MTS. Results Elisa assay displayed that the protein level of IL-6 of TAM/LoVo-P was higher than TAM/LoVo-C. Wound healing and MTS test both displayed that the migration and proliferation of LoVo-P were higher than LoVo-C when co-culture with TAM.Western blot reminded the proteins of p-AKT and p-STAT3 in LoVo-P were higher than LoVo-C after co-culture with TAMs. When we added different dosages of IL- 6 （1,10,100 NG/ML） in culture medium of LoVo-P, the migration and proliferation were increased gradually, also the proteins of p-AKT and p-STAT3 gradient increased. Conclusion PRL-3 promotes colon cancer cells proliferation and migration depends on paracrine IL-6 signaling and up-regulate the proteins of p-AKT and p-STAT3.

关 键 词：肝再生磷酸酶-3 结肠癌 白介素6 迁移 

分 类 号：R735.35[医药卫生—肿瘤]