幽门螺杆菌通过Wnt/β-catenin信号通路对胃癌细胞侵袭及血管新生因子的作用研究

Study on helicobacter pylori regulating invasion of gastric cancer cells and angiogenesis factors through Wnt/β-catenin pathway

摘要:

目的 研究幽门螺杆菌（Hp）通过Wnt/β-catenin信号通路对胃癌细胞侵袭及血管新生因子的作用。方法 收集手术切除的胃癌组织并检测Wnt1、Wnt3a、β-catenin、MMP-7、N-cadherin、E-cadherin、VEGF、bFGF、Ang-2 mRNA的相对表达量。培养胃癌细胞株SGC-7901，分为对照组、Hp组、Hp + ICG-001组。对照组用不含细菌及药物的DMEM处理，Hp组用含有Hp的DMEM处理，Hp + ICG-001组用含有Hp及Wnt/β-catenin信号通路抑制剂ICG-001的DMEM处理。采用Western blotting检测Wnt1、Wnt3a、β-catenin、MMP-7、N-cadherin、E-cadherin蛋白的相对表达量。采用Transwell检测侵袭数目。采用酶联免疫吸附试验检测VEGF、bFGF、Ang-2的含量。结果 与Hp阴性胃癌组织比较，Hp阳性胃癌组织中Wnt1、Wnt3a、β-catenin、MMP-7、N-cadherin、VEGF、bFGF、Ang-2 的mRNA相对表达量均增加（P <0.05），E-cadherin 的mRNA相对表达量降低（P <0.05）；Hp组Wnt1、Wnt3a、β-catenin、MMP-7、N-cadherin蛋白相对表达量、侵袭数目、VEGF、bFGF、Ang-2的含量高于对照组（P <0.05），E-cadherin的相对表达量低于对照组（P <0.05）；Hp + ICG-001组Wnt1、Wnt3a、β-catenin、MMP-7、N-cadherin蛋白相对表达量、侵袭数目、VEGF、bFGF、Ang-2的含量低于Hp组（P <0.05），E-cadherin的相对表达量高于Hp 组（P <0.05）。结论 Hp通过Wnt/β-catenin信号通路促进胃癌细胞的侵袭及血管新生因子生成。

Abstract:

Objective To study the role of helicobacter pylori (Hp) in regulating the invasion and of gastric cancer cells angiogenesis factors through Wnt/β-catenin pathway.Methods Gastric cancer cell line SGC-7901 were divided into control group, Hp group, and Hp+ICG-001 group. The control group was treated with DMEM without bacteria and drugs, Hp group was treated with DMEM containing Hp and Hp+ICG-001 was treated with DMEM containing Hp and Wnt/β-catenin pathway inhibitor ICG-001. The expression of Wnt1, Wnt3a, β-catenin, MMP-7, N-cadherin, and E-cadherin were measured by Western blotting, the number of invasion was measured by Transwell, and the contents of VEGF, bFGF, Ang-2 were measured by ELISA.Results Compared with Hp-negative gastric cancer, the mRNA expression of Wnt1, Wnt3a, β-catenin, MMP-7, N-cadherin, VEGF, bFGF, and Ang-2 in Hp-positive gastric cancer significantly increased, while that of E-cadherin significantly decreased (P < 0.05). The expression of Wnt1, Wnt3a, β-catenin, MMP-7, N-cadherin, invasion number, the contents of VEGF, bFGF, Ang-2 in Hp group were higher than those in control group, and the expression of E-cadherin was lower than that in control group (P < 0.05); the expression of Wnt1, Wnt3a, β-catenin, MMP-7, N-cadherin, invasion number, the contents of VEGF, bFGF, Ang-2 in Hp+ICG-001 group were lower than those in Hp group, and the expression of E-cadherin was higher than that in Hp group (P < 0.05).Conclusion Hp can promote the invasion of gastric cancer cells and angiogenesis factor production through Wnt/β-catenin pathway.