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岭南现代临床外科 ›› 2016, Vol. 16 ›› Issue (05): 517-520.DOI: 10.3969/j.issn.1009-976X.2016.05.002

• 论著与临床研究 • 上一篇    下一篇

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

来伟 施景龙 林显敢 许鹤洋 蓝球生 褚忠华   

  1. 中山大学孙逸仙纪念医院
  • 通讯作者: 褚忠华

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

LAI Wei, SHI Jinglong, LIN Xiangan, XU Heyang, LAN Qiusheng, CHU Zhonghua   

  • Online:2016-10-20 Published:2016-10-20
  • Contact: CHU Zhonghua

摘要: 【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LoVo-Control(LoVo-C)结肠癌细胞和稳定表达PRL-3的实验组LoVo-PRL-3 (LoVo-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/LoVo-P(102±5)PG/ML,TAM/LoVo-C为(56±3)PG/ML;划痕实验与MTS结果均提示共培养后LoVo-P增殖、侵袭能力比LoVo-C强;Western blot 检测共培养后的结肠癌细胞LoVo-P、LoVo-C蛋白表达差异,p-AKT、p-STAT3表达LoVo-P明显高于LoVo-C,不同浓度的IL-6(1、10、100 NG/ML)作用LoVo-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。

关键词: 白介素6, 肝再生磷酸酶-3, 结肠癌, 迁移

Abstract: 【Abstract】 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.

Key words: IL-6, Colon cancer, PRL-3, Migration

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