| 刘涛.MIF调控GNG7/β-catenin信号通路促进I型幽门螺杆菌诱导的胃癌细胞干性[J].安徽医药,待发表. |
| MIF调控GNG7/β-catenin信号通路促进I型幽门螺杆菌诱导的胃癌细胞干性 |
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| 投稿时间：2025-03-14 录用日期：2025-04-18 |
| DOI： |
| 中文关键词: MIF GNG7/β-catenin I型幽门螺杆菌 干性 |
| 英文关键词: |
| 基金项目:铜川市医学会2023年第一届科研课题项目（202301a02）； 铜川市科学技术局2023年度科学技术研究发展计划项目 |
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| 中文摘要: |
| 目的:基于GNG7/β-catenin信号通路,探究MIF介导I型幽门螺杆菌(I型HP)诱导的胃癌细胞干性的机制。方法:将胃癌细胞AGS分为siRNA MIF-NC组、siRNA MIF组、Hp+siRNA MIF-NC组、Hp+siRNA MIF组、Hp+si-MIF+si-GNG7组,MTT实验检测胃癌细胞活性,划痕实验检测胃癌细胞迁移能力,Transwell实验检测胃癌细胞侵袭能力,成球实验检测胃癌细胞的干性,Western blot检测干性指标有机阳离子/肉碱转运体(OCT-4)、CD44、Nanog同源盒(Nanog)、SRY-box转录因子2(SOX-2)、GNG7、GSK-3β、β-catenin的蛋白表达。结果:相对于siRNA MIF-NC组,siRNA MIF组胃癌细胞的细胞活性显著降低(P<0.05),迁移、侵袭能力显著降低(P<0.05),OCT-4、CD44、Nanog、SOX-2、β-catenin蛋白的表达显著下调(P<0.05),GNG7、GSK-3β表达显著上调(P<0.05)；相对于siRNA MIF-NC组,Hp+siRNA MIF-NC组胃癌细胞的细胞活性显著增加(P<0.05),迁移、侵袭能力显著提升(P<0.05),OCT-4、CD44、Nanog、SOX-2、β-catenin蛋白的表达显著上调(P<0.05),GNG7、GSK-3β表达显著下调(P<0.05)；相对于Hp+siRNA MIF-NC组,Hp+siRNA MIF组胃癌细胞的细胞活性显著降低(P<0.05),迁移、侵袭能力显著降低(P<0.05),OCT-4、CD44、Nanog、SOX-2、β-catenin蛋白的表达显著下调(P<0.05),GNG7、GSK-3β表达显著上调(P<0.05)；相对于Hp+siRNA MIF组,Hp+si-MIF+si-GNG7组胃癌细胞的迁移、侵袭能力显著提升(P<0.05),OCT-4、CD44、Nanog、SOX-2蛋白的表达显著上调(P<0.05)。结论:MIF通过调控GNG7/β-catenin信号通路促进I型HP诱导的胃癌细胞干性。 |
| 英文摘要: |
| Objective: Based on GNG7/β-catenin signaling pathway, the mechanism of MIF mediating Helicobacter pylori type I (Helicobacter pylori type I) induced gastric cancer cell xerogenicity was explored. Methods: Gastric cancer cells AGS were divided into siRNA MIF-NC group, siRNA MIF group, Hp+siRNA MIF-NC group, Hp+siRNA MIF group,? Hp+si-MIF+si-GNG7 group. The activity of gastric cancer cells was detected by MTT assay. The scratch assay was used to detect the migration ability of gastric cancer cells.? The Transwell assay was used to detect the invasion ability of gastric cancer cells The dryness of gastric cancer cells was detected by pelleting assay. The dry index of organic cationic carnitine transport (OCT-4), CD44, Nanog homeobox (Nanog), SRY-box transcription factor 2(SOX-2), and GNG7, GSK-3β, β-catenin were detected by Western blot.Results: Compared with the siRNA MIF-NC group, the cell activity and migration and invasion ability of gastric cancer cells in the siRNA MIF group were significantly decreased (P<0.05), and the expression of OCT-4, CD44, NanogSOX-2, β-catenin protein were significantly down-regulated (P<0.05), and the expression of GNG7, GSK-3β was significantly increased (P<0.05). Compared with the siRNA MIF-NC group, the cell activity and migration and invasion ability of gastric cancer cells in Hp+siRNA MIIF-NC group were significantly increased (P<0.05), and the expression of OCT-4, CD44, NanogSOX-2, β-catenin protein were significantly up-regulated (P<0.05), and the expression of GNG7, GSK-3β was significantly decreased (P<0.05). Compared with Hp+siRNA MIF-NC group, the cell activity and migration and invasion ability of gastric cancer cells in Hp+siRNA MIF group were significantly decreased (P<0.05), and the expression of OCT-4, CD44, NanogSOX-2, β-catenin protein were significantly down-regulated (P<0.05), and the expression of GNG7, GSK-3β was significantly increased (P<0.05). Compared with Hp+siRNA MIF group, the migration and invasion ability of gastric cancer cells in Hp+si-MIF+si-GNG7 group was significantly improved (P<0.05), and the expression of OCT-4, CD44, Nanog, SOX-2 proteins were significantly up-regulated (P<0.05).Conclusion: MIF promotes Helicobacter pylori type I-induced stemness of gastric cancer cells by regulating the GNG7/β-catenin signaling pathway. |
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