吲哚美辛通过E-Cad逆转高糖诱导的胰腺癌细胞增殖作用

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。

Indometacin ameliorates high glucose-induced proliferation via modulation of E-cadherin in pancreatic cancer cells

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 expression 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 regulated 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.