Qian Xuemin, Huang Camy, Cho Chi Hin, Hui Wai Mo, Rashid Asif, Chan Annie On On
Division of Gastroenterology and Hepatology, Department of Medicine, University of Hong Kong, Hong Kong.
Cancer Lett. 2008 May 8;263(1):107-13. doi: 10.1016/j.canlet.2007.12.023. Epub 2008 Feb 4.
Interleukin-1beta is up-regulated in the presence of Helicobacter pylori infection. H. pylori infection was associated with E-cadherin methylation. In this study, we examined if IL-1beta could induce promoter methylation of E-cadherin in human gastric cancer cell lines TMK-1, MKN-74 and MKN-7. Cells were treated with IL-1beta (0.025, 0.1, 0.25, 1.0, 2.5 ng/mL) for 6, 12 and 24h. Methylation status was determined by MSP and sequencing. The effects of IL-1beta or H.pylori on the cells, and after blockade with interleukin-1 receptor antagonist (IL-1ra) were tested. Promoter methylation of E-cadherin was induced in all three cells treated with IL-1beta or co-cultured with H. pylori. Treatment of IL-1ra could reverse the phenomena. Our study indicated that IL-1beta is an important step in mediating E-cadherin methylation.
白细胞介素-1β在幽门螺杆菌感染时上调。幽门螺杆菌感染与E-钙黏蛋白甲基化有关。在本研究中，我们检测了白细胞介素-1β是否能诱导人胃癌细胞系TMK-1、MKN-74和MKN-7中E-钙黏蛋白的启动子甲基化。细胞用白细胞介素-1β（0.025、0.1、0.25、1.0、2.5 ng/mL）处理6、12和24小时。通过甲基化特异性PCR（MSP）和测序确定甲基化状态。检测了白细胞介素-1β或幽门螺杆菌对细胞的影响，以及用白细胞介素-1受体拮抗剂（IL-1ra）阻断后的影响。用白细胞介素-1β处理或与幽门螺杆菌共培养的所有三种细胞中均诱导了E-钙黏蛋白的启动子甲基化。用IL-1ra处理可逆转这些现象。我们的研究表明，白细胞介素-1β是介导E-钙黏蛋白甲基化的重要环节。
