| 刘涛,王剑锋,杨冰,等.巨噬细胞移动抑制因子调控 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,2026,30(9):1853-1860. |
| 巨噬细胞移动抑制因子调控 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 |
| MIF promotes the stemness of gastric cancer cells induced by Helicobacter pylori type Ⅰ by the regulation of GNG7/β-catenin signaling pathway |
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| DOI：10.3969/j.issn.1009-6469.2026.09.029 |
| 中文关键词: 胃肿瘤 巨噬细胞移动抑制因子 G蛋白亚基 γ7 β-联蛋白 Ⅰ型幽门螺杆菌 干性 |
| 英文关键词: Stomach neoplasms Macrophage migration inhibition factor G protein subunit γ7 β-catenin Helicobacter pylori type Ⅰ Stemness |
| 基金项目:铜川市科学技术局 2023年度科学技术研究发展计划社发攻关项目( 1)；铜川市医学会第一届科研课题项目(202301a02) |
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| 中文摘要: |
| 目的基于 G蛋白亚基 γ7(GNG7)/β-联蛋白( β-catenin)信号通路，探究巨噬细胞移动抑制因子( 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。方法于 2024年 2—12月体外培养胃癌 AGS细胞，分为干扰小 RNA(siRNA) MIF-阴性对照(NC)组(siRNA MIF-NC转染)、siRNA MIF组(siRNA MIF转染)、Hp+siRNA MIF-NC组(Ⅰ型 Hp感染 +siRNA MIF-NC转染)、 Hp+siRNA MIF组(Ⅰ型 Hp感染 +siRNA MIF转染)、 Hp+si-MIF+si-GNG7组(Ⅰ型 Hp感染 +siRNA MIF转染 +siRNA GNG7转染)。噻唑蓝( 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，蛋白质印迹法检测干性指标有机阳离子 /肉碱转运体( OCT-4)、分化抗原 44(CD44)、 Nanog同源盒(Nanog)、 SRY-box转录因子 2(SOX-2)及 GNG7、糖原合成酶激酶 -3β(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(0.16±0.01比 0.28±0.02)、 CD44(0.19±0.01比 0.31±0.03)、 Nanog(0.21±0.02比 0.34±0.0，3)、 SOX-2(0.19±0.01比 0.38±0.03)、β，-catenin(0.25±0.02比 0.37±0.04)蛋白的表达显著下调( P<0.05)GNG7(0.81±0.06比 0.43±0.03)、 GSK-3β(0.84±0.07比 0.41±0.03)表达显著上调( P< 0.05)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(0.89±0.06比 0.28±0.0，2)、 CD44(0.83±0.07比 0.31±0.03)、 Nanog(0.93±0.08比 0.34±0.03)、S，OX-2(0.86±0.07比 0.38±0.03)、β，-catenin(0.82±0.08比 0.37±0.04)蛋白的表达显著上调( P<0.05)，GNG7(0.18±0.01比 0.43±0.03)、 GSK-3β(0.22±0.02比 0.41±0.03)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(0.43±0.03比 0.89±0.06)CD44(0.39±0.03比 0.83±0.07)Nanog(0.48±0.04比 0.93±0.08)，SOX-2(0.32±0.03比 0.86± 0.07)、β，-catenin(0.51±0.04比0.82±0.08)、蛋白的表达显著下调( P<0.05)、，GNG7(0.36±0.03比 0.18±0.01、)、 GSK-3β(0.47±0.03比 0.22±0.02)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(0.57±0.05比 0.24±0.02)、CD44(0.53±0.04比 0.29±0.02)Nanog(0.65±0.05比 0.17±0.01)SOX-2(0.52±0.04比 0.13±0.01白的表达显著上调( P<0.05)。结论 enin信号通路促进 Ⅰ型 Hp诱的胃癌细胞干性。 |
| 英文摘要: |
| Objective To investigate the mechanism of macrophage migration inhibition factor (MIF) mediating Helicobacter pyloritype Ⅰ (type Ⅰ Hp) induced gastric cancer cell xerogenicity based on G protein subunit γ7 (GNG7)/β -catenin signaling pathway. Methods From February to December 2024, AGS gastric cancer cells were cultured in vitro and divided into the siRNA MIF-NC group (transfected with siRNA MIF-NC), the siRNA MIF group (transfected with siRNA MIF), the Hp siRNA MIF-NC group (type Ⅰ Hp-infected, transfected with siRNA MIF-NC), the Hp siRNA MIF group (type Ⅰ Hp-infected, transfected with siRNA MIF), and the Hp si-MIF si-GNG7 group (type Ⅰ Hp-infected, transfected with siRNA MIF and siRNA GNG7). The activity of gastric cancer cellswas detected by thiazolyl blue (MTT) assay. The scratch assay was used to detect the migration ability of gastric cancer cells. The Tran. swell assay was used to detect the invasion ability of gastric cancer cells. The dryness of gastric cancer cells was detected by pelletingassay. The dry index of organic cationic carnitine transport (OCT-4), cluster of differentiation 44 (CD44), Nanog homeobox (Nanog), SRY-box transcription factor 2 (SOX-2), and GNG7, glycogen synthase kinase-3β (GSK-3β), β-catenin were detected by Western blot. ting.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 significantly decreased (P<0.05), and the expression of OCT-4 (0.16±0.01 vs. 0.28±0.02), CD44 (0.19±0.01 vs. 0.31±0.03), Nanog (0.21±0.02 vs. 0.34±0.03), SOX-2 (0.19±0.01 vs. 0.38±0.03), β -catenin (0.25±0.02 vs. 0.37±0.04) protein signifi. cantly down-regulated (P<0.05), and the expression of GNG7 (0.81±0.06 vs. 0.43±0.03), GSK-3β (0.84±0.07 vs. 0.41±0.03) significant. ly 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 MIF-NC group significantly increased (P<0.05), and the expression of OCT-4 (0.89±0.06 vs. 0.28±0.02), CD44 (0.83±0.07 vs. 0.31±0.03), Nanog (0.93±0.08 vs. 0.34±0.03), SOX-2 (0.86±0.07 vs. 0.38±0.03), β -catenin (0.82±0.08 vs. 0.37±0.04) protein significantly up-regulated (P<0.05), and the expression of GNG7 (0.18±0.01 vs. 0.43±0.03), GSK-3β (0.22±0.02 vs. 0.41±0.03) significantly decreased (P<0.05). Compared with Hp+siRNA MIF-NC group, the cell activity and migration and invasion ability of gas.tric cancer cells in Hp+siRNA MIF group significantly decreased (P<0.05), and the expression of OCT-4 (0.43±0.03 vs. 0.89±0.06), CD44 (0.39±0.03 vs. 0.83±0.07), Nanog (0.48±0.04 vs. 0.93±0.08), SOX-2 (0.32±0.03 vs. 0.86±0.07), β-catenin (0.51±0.04 vs. 0.82± 0.08) protein significantly down-regulated (P<0.05), and the expression of GNG7 (0.36±0.03 vs. 0.18±0.01), GSK-3β (0.47±0.03 vs. 0.22±0.02) 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 significantly improved (P<0.05), and the expression of OCT-4 (0.57±0.05 vs. 0.24±0.02), CD44 (0.53±0.04 vs. 0.29±0.02), Nanog (0.65±0.05 vs. 0.17±0.01), SOX-2 (0.52±0.04 vs. 0.13±0.01) proteins significantly up-regulated (P< 0.05).Conclusion MIF promotes the stemness of gastric cancer cells induced by type Ⅰ Hp by regulating the GNG7/β-catenin signal. ing pathway. |
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