姜黄素对人肺癌A549细胞增殖的影响及机制  被引量:6

Effect of curcumin on the proliferation of human lung cancer cell A549 and the mechanisms

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作  者:王林辉[1] 张雄 陈慧勇 杜日昌[1] 高双全[1] 张莹 谭彩云[1] WANG Lin-hui;ZHANG Xiong;CHEN Hui-yong;DU Ri-chang;GAO Shuang-quan;ZHANG Ying;TAN Cai-yun(Department of Pathology,the Affiliated YUE BEI Peoples'Hospital of Shantou Medical University Shaoguan 512026,Guangdong,China)

机构地区:[1]粤北人民医院病理科,广东韶关512026 [2]粤北人民医院胸外科,广东韶关512026 [3]重庆医科大学基础医学院神经科学研究中心,重庆400016

出  处:《广东医学》2019年第23期3233-3239,共7页Guangdong Medical Journal

基  金:韶关市卫生计生科研项目(编号:Y19037)

摘  要:目的探讨姜黄素对肺癌A549细胞增殖的影响,并探讨其机制。方法体外培养肺癌A549细胞,用不同浓度的姜黄素(5、10、20、40μmol/L)处理不同的时间(24、48和72 h)。采用MTT检测姜黄素对细胞增殖活力的影响。然后,采用脂质体法向A549细胞转染质粒pCDNA3.1和pCDNA3.1-ILK,用姜黄素20μmol/L处理细胞,采用MTT法检测细胞增殖活性,荧光定量PCR(qRT-PCR)法检测细胞中整合素连接激酶(ILK)、β-连环蛋白(β-catenin)和血管内皮生长因子(VEGF)的mRNA水平;Western blot法检测细胞中ILK、β-catenin、VEGF蛋白的表达。结果与空白对照组比较,随着姜黄素浓度的增加和作用时间的延长,A549细胞的增殖率明显受到抑制,存在剂量-时间依赖性(P<0.05);而细胞中的ILK、β-catenin、VEGF mRNA和蛋白表达水平都显著降低;而过表达ILK后,细胞的增殖活性显著增高(P<0.05),且细胞中的ILK、β-catenin、VEGF mRNA和蛋白表达水平又显著增高(P<0.05)。结论姜黄素可通过调节ILK的活性进而抑制肺癌细胞的增殖,其可能的机制与姜黄素使Wnt/β-catenin信号通路失活,并降低下游靶基因VEGF的表达有关。Objective To observe the effects of curcumin on cell proliferation of A549 cells, and to explore its potential mechanism. Methods A549 cells were cultured in vitro and treated with different concentrations of curcumin(5, 10, 20 and 40 μmol/L) for 24, 48 and 72 hours. MTT assay was used to assess cell proliferation. The cells were transfected with pcDNA3.1 and pcDNA3.1-ILK by liposome method, and treated with curcumin by 20 μmol/L. The cell inhibitory rate of the cells were assessed by MTT, the expression of integrin-linked kinase(ILK), β-catenin and vascular endothelial growth factor(VEGF) at mRNA and protein levels were determined by qRT-PCR and Western blot, respectively.Results Compared with the blank control group, 20 μmol/L curcumin treatment for 24 hours significantly inhibited the proliferation of the lung cancer A549 cells a concentration-time dependent manner(P<0.05). The expression of ILK, β-catenin and VEGF at mRNA and protein levels were all significantly reduced(P<0.05). After overexpression of ILK, the proliferation rate of A549 cells was significantly enhanced(P<0.05), and the expression of ILK, β-catenin and VEGF mRNA and protein were significantly increased(P<0.05). Conclusion Curcumin could inhibit the proliferation of lung cancer cells A549 by regulating the activity of ILK, and its possible mechanism may be related that curcumin inactivates the Wnt/β-catenin signaling pathway, and reduces the expression of the downstream target VEGF.

关 键 词:肺癌 姜黄素 整合素蛋白激酶 Β-连环蛋白 血管内皮生长因子 

分 类 号:R734.2[医药卫生—肿瘤] R979[医药卫生—临床医学]

 

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