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OALib Journal期刊
ISSN: 2333-9721
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-  2016 

全反式维甲酸联合LY294002对食管癌EC1细胞增殖、迁移及PI3K、MMP-2表达的影响
Effect of all??trans retinoic acid combined with LY294002 on proliferation,migration and expressions of PI3K and MMP??2 in EC1cells

Keywords: 全反式维甲酸,LY294002,EC1细胞,PI3K,MMP??2
sall??trans retinoic acid
,LY294002,EC1 cell,phosphoinositide 3??kinase,matrix metalloproteinase??2

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Abstract:

目的:探讨全反式维甲酸(ATRA)、磷脂酰肌醇激酶??3(PI3K)抑制剂LY294002单独或联合作用对食管癌EC1细胞增殖、迁移及PI3K和MMP??2表达的影响。方法:将常规培养的EC1细胞随机分为ATRA组、LY294002组、ATRA+LY294002组和对照组4组,采用CCK??8检测各组细胞的增殖情况,通过划痕实验测定各组细胞的迁移能力,采用RT??PCR和Western blot方法检测各组细胞中PI3K及MMP??3 mRNA和蛋白的表达情况。结果:作用24、48和72 h后,ATRA+LY294002组的细胞增殖抑制率均高于其他2组(P<0.05);作用24 h后,ATRA+LY294002组细胞迁移能力均低于其他3组(P<0.05);作用48 h后,ATRA+LY294002组细胞PI3K及MMP??2 mRNA和蛋白的表达量均低于其他3组(P<0.05)。结论:ATRA联合LY294002可协同抑制EC1细胞的增殖、迁移和PI3K、MMP??2的表达,进而可能协同抑制肿瘤血管生成。
Aim: To investigate effects of all??trans retinoic acid(ATRA),LY294002 alone or combined on proliferation,migration and phosphoinositide 3??kinase(PI3K),matrix metalloproteinase??2(MMP??2) expressions of EC1 cells in vitro.Methods: The cultured EC1 cells were randomly allocated into four groups: ATRA group, LY294002 group, ATRA plus LY294002 group and control group. The proliferation rate was detected by CCK??8 assay. Wound healing assay was used to observe the migration rate. The mRNA and protein expressions of PI3K and MMP??2 in the cells were detected by RT??PCR and Western blot assay.Results: The cell proliferation inhibition rate of ATRA plus LY294002 was higher than those of the other three groups after 24,48, and 72 h treatment(P<0.05). The migration rate of ATRA plus LY294002 group was lower than those of the other three groups after 24 h treatemnt(P<0.05). The relative expressions of PI3K and MMP??2 mRNA and protein of ATRA plus LY294002 group were lower than those of the other three groups after 48 h treatment(P<0.05).Conclusion: ATRA combined with LY294002 could inhibit EC1 cells′ proliferation, migration and the expressions of PI3K and MMP??2, which may be related to the inhibition of tumor angiogenesis

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