Prostaglandin E2 upregulates ICAM-1 expression and activity in HuCCT1 cells via the EP2 receptor signaling pathway
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    Abstract:

    Objective:To investigate the effect of prostaglandin E2(PGE2) on the expression of intercellular adhesion molecule-1 (ICAM-1) and the cell migration ability by EP2 receptor in cholangiocarcinoma HuCCT1 cells. Methods: HuCCT1 cells were treated with PGE2,EP1-4 receptor agonist,EP2 receptor antagonist,AC inhibitor,and protein kinase A (PKA) inhibitor. Western blotting and scratch assay were employed to detect the protein level of ICAM-1 and the cell migration ability in HuCCT1 cells. Results: PGE2 might upregulate the protein level of ICAM-1 in cholangiocarcinoma HuCCT1 cells. The protein level of ICAM-1 was increased by 66.17%(P < 0.05) compared with the control group after treatment with 5 -滋mol/L PGE2 for 24 h,and the increase was dose- and time-dependent. The cell migration ability of HuCCT1 was increased by 43.29% (P < 0.01) compared with the group after treated with 5 -滋mol/L PGE2. The protein expression of ICAM-1 in HuCCT1 cells were increased by 257.88%(P < 0.05) after treatment with EP2 receptor agonist for 24 h,and the cell migration ability of HuCCT1 was increased by 56.99%(P < 0.01). The protein level of ICAM-1 decreased by 49.14% (P < 0.05) compared with the group,which were treated with PGE2 after treatment with 10 -滋mol/L EP2 receptor antagonist,and the cell migration ability of HuCCT1 decreased by 52.06% (P < 0.01). When treated with 25 -滋mol/L AC inhibitor SQ22536 and 10 -滋mol/L PKA antagonist H89 for 24h,the protein levels of ICAM-1 were decreased by 72.87%(P < 0.05),80.78%(P < 0.05) compared with the group treated with EP2 receptor agonist. Conclusion: PGE2 upregulates the protein level of ICAM-1 and the cell migration ability through EP2 receptor in cholangiocarcinoma HuCCT1 cells,which could be partly related to the cAMP-PKA signaling pathway.

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许 燕,白小明,张 丽,马 娟,张 海,汪亦品,冷 静. EP2受体介导的前列腺素E2影响胆管细胞癌细胞HuCCT1细胞间黏附因子-1表达和侵袭的研究[J].南京医科大学学报(自然科学版英文版),2012,(5):592-597.

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  • Received:December 28,2011
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