吲哚美辛通过E－Cad逆转高糖诱导的胰腺癌细胞增殖作用

摘要

目的:研究吲哚美辛对高糖环境下胰腺癌细胞增殖能力的影响,并探讨相关机制.方法:体外培养胰腺癌细胞株BXPC－3和Panc－1,应用MTT法检测肿瘤细胞在不同干预条件下的增殖能力;应用Real time－PCR和Western blot检测细胞中E－Cad和COX－2的表达.应用小干扰RNA敲除肿瘤细胞中E－Cad的表达.结果:高糖可促进胰腺癌细胞增殖能力;而吲哚美辛可逆转高糖条件促进胰腺癌细胞的增殖,同时吲哚美辛可调控肿瘤细胞中E－Cad的表达,且小干扰胰腺癌细胞E－Cad后可逆转吲哚美辛对高糖引起的增殖抑制作用.结论:吲哚美辛可以抑制高糖诱导的胰腺癌细胞增殖,且该过程是通过上调E－Cad实现的,而非通过COX－2途径.%Objective:To investigate the effect and mechanism of indometacin on high glucose(HG)－induced proliferation of pancreatic cancer(PC)cells.Methods:The human PC cell lines,BXPC－3 and Panc－1,were used in vitro.MTT assay was carried to examine the proliferation ability in PC cells in different concentrations.The expres-sion of E－Cad and COX－2 in PC cells were detected by RT－PCR and Western blot analysis.siRNA was used to knockdown E－Cad in PC cells.Results:HG could increase the proliferation rate of PC cells.Then indometacin could down－regulated the effect of HG－induced proliferation in PC cells.The expression of E－Cad in PC cells was regu-lated by indometacin.The proliferation rate of PC cells incubated in HG of indometacin was increased in cells that the E－Cad was knockdown by siRNA.Conclusion:Indometacin could suppress the effect of HG－induced proliferation in PC cells by up－regulating the expression of E－Cad.