实用肿瘤学杂志 ›› 2019, Vol. 33 ›› Issue (3): 228-232.doi: 10.11904/j.issn.1002-3070.2019.03.007

• 基础研究 • 上一篇    下一篇

m白术内酯Ⅰ通过TLR4/MyD88通路调控肺癌A549细胞增殖侵袭的研究

刘志强1,褚艳杰2,刘静2,王彦博3   

  1. 1.哈尔滨医科大学附属肿瘤医院血液科(哈尔滨 150081);
    2.哈尔滨医科大学附属第二医院消化内科;
    3.哈尔滨医科大学附属肿瘤医院胸外科
  • 收稿日期:2019-03-20 修回日期:2019-05-08 出版日期:2019-06-20 发布日期:2019-06-18
  • 通讯作者: 王彦博,E-mail:wangyanbo_034@126.com
  • 作者简介:刘志强,男,(1981-),硕士,住院医师,从事恶性肿瘤化学治疗的研究

Atractylenolide I regulates proliferation and invasion of lung cancer A549 cells through the TLR4/MyD88 pathway

LIU Zhiqiang1,CHU Yanjie2,LIU Jing2,WANG Yanbo3   

  1. 1.Department of Hematology,Harbin Medical University Cancer Hospital,Harbin 150081,China;
    2.Department of Gastroenterology and Hepatology,The Second Affiliated Hospital of Harbin Medical University;
    3.Department of Thoracic Surgery,Harbin Medical University Cancer Hospital
  • Received:2019-03-20 Revised:2019-05-08 Online:2019-06-20 Published:2019-06-18

摘要: 目的 探究白术内酯Ⅰ在肺癌进程中的作用及分子机制。方法 用qRT-PCR和免疫组化实验检测肺癌组织和癌旁组织中TLR4及MyD88的mRNA和蛋白的表达;Transwell侵袭实验及MTT实验检测白术内酯Ⅰ(100 μM/L)对A549细胞侵袭、增殖能力的影响;Western blot检测白术内酯Ⅰ对TLR4及MyD88蛋白表达的作用。结果 qRT-PCR及免疫组化结果显示,相对于癌旁组织,TLR4及MyD88的mRNA和蛋白在肺癌组织中高表达(P<0.05);与对照组相比,白术内酯Ⅰ处理组A549细胞侵袭能力显著下降,增殖活力显著抑制(P<0.05);Western blot结果显示,白术内酯Ⅰ抑制TLR4及MyD88蛋白表达水平(P<0.05)。结论 白术内酯Ⅰ通过抑制TLR4/MyD88通路抑制肺癌A549细胞侵袭转移。

关键词: 白术内酯Ⅰ, 肺癌A549细胞, TLR4/MyD88, 增殖, 侵袭

Abstract: Objective The Objective of this study was to investigate the role and molecular mechanism of Atractylenolide Ⅰ in the progression of lung cancer.Methods qRT-qPCR and immunohistochemistry were used to detect the expression of TLR4 and MyD88 at levels of mRNA and protein in lung cancer and adjacent tissues.Transwell and MTT assays were used to detect effects of atractylenolide I(100 μM)on the invasion,migration and proliferation of A549 cells.Western blot was also used to detect the effect of atractylenolide I on the expression of TLR4 and MyD88 proteins.Results The expression of TLR4 and MyD88 at levels of mRNA and protein was highly expressed in lung cancer tissues when compared to adjacent tissues(P<0.05).Compared with the control group,the invasion ability of A549 cells in the Atractylenolide I group was significantly decreased,and the proliferative activity was inhibited(P<0.05).Atractylenolide I inhibited the expression of TLR4 and MyD88 protein in A549 cells(P<0.05).Conclusion Atractylenolide I inhibits the invasion and metastasis of lung cancer A549 cells by inhibiting the TLR4/MyD88 pathway.

Key words: Atratcylenolide I, Lung cancer A549 cells, The TLR4/MyD88 pathway, Proliferation, Invasion

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