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罗格列酮对肝癌SMMC-7721细胞VEGF蛋白表达的影响[J]. 肿瘤防治研究, 2010, 37(03): 298-300. DOI: 10.3971/j.issn.1000-8578.2010.03.015
引用本文: 罗格列酮对肝癌SMMC-7721细胞VEGF蛋白表达的影响[J]. 肿瘤防治研究, 2010, 37(03): 298-300. DOI: 10.3971/j.issn.1000-8578.2010.03.015
Effect ofRosiglitazone onExpression ofVEGF in LiverCancerCellLine SMMC-7721[J]. Cancer Research on Prevention and Treatment, 2010, 37(03): 298-300. DOI: 10.3971/j.issn.1000-8578.2010.03.015
Citation: Effect ofRosiglitazone onExpression ofVEGF in LiverCancerCellLine SMMC-7721[J]. Cancer Research on Prevention and Treatment, 2010, 37(03): 298-300. DOI: 10.3971/j.issn.1000-8578.2010.03.015

罗格列酮对肝癌SMMC-7721细胞VEGF蛋白表达的影响

Effect ofRosiglitazone onExpression ofVEGF in LiverCancerCellLine SMMC-7721

  • 摘要: 目的 探讨过氧化物酶体增殖激活物受体γ( PPARγ) 配体罗格列酮对肝癌SMMC-7721细胞中VEGF表达的影响及其可能机制。 方法 经不同浓度罗格列酮(0、0.1、1、10、100μmol/L)分别作用SMMC-7721细胞24h、48h、72h 后,采用Western印迹法检测细胞VEGF和PTEN、Akt1/2及P-Akt1蛋白表达的变化。 结果 罗格列酮可以显著抑制SMMC-7721细胞中VEGF蛋白表达水平(P<0.05),呈时间和剂量依赖性;能上调细胞PTEN的表达,并呈时间和剂量依赖性(P<0.05),但Akt1/2及P-Akt1的表达无明显改变(P>0.05)。 结论 罗格列酮可抑制SMMC-7721细胞中VEGF蛋白表达,该作用可能是与上调PTEN表达有关,但不是通过直接抑制PI3K/Akt信号转导途径来实现的。

     

    Abstract: Objective To study theeffects of rosiglitazone ligands of peroxisome proliferator-activated receptor-γ(PPAR-γ) on theexpression of VEGF in hepatocellular carcinoma cell lineSMMC-7721,in vitro andto reveal therelated molecular mechanisms. Methods After treatment with different concentration of rosiglitazone (0, 0.1, 1,10 and 100μmol/L) for different time(24h, 48hand72h), the expressions of VEGF,PTEN, Akt1/2 and P-Akt1 were detected by western blot. Results Rosiglitazonecouldsignificantlyinhibitthe expression of VEGF in SMMC-7721 cells and have both time-dependent and concentration-dependent manner (P<0.05).Rosiglitazone increasedthe expression ofPTEN remarkably inboth time-dependent and concentration-dependent manner(P<0.05), but has no influence on theexpression of Akt1/2 and P-Akt1. Conclusion This study suggested that activation of PPARγ by rosiglitazone can inhibit the expression of VEGF, which may be through the upregulation the expression level of PTEN while not directly relyingon PI3K/Akt.

     

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