幽门螺杆菌通过糖皮质激素受体调节巨噬细胞极化，促进胃癌细胞增殖

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY

Tissue & cell Pub Date : 2025-05-31 DOI:10.1016/j.tice.2025.103001

Xiuping Wang , Yiwei Weng , Yongliang Yao , Shihe Shao , Lingxiang Mao , Jianjun Wang

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引用次数: 0

摘要

背景幽门螺杆菌（h.p ylori）被认为是胃癌（GC）的主要危险因素。然而，幽门螺杆菌在癌症进展中影响巨噬细胞免疫反应的确切机制仍然知之甚少。本研究探讨幽门螺杆菌如何通过糖皮质激素受体（NR3C1）影响巨噬细胞极化及其在胃癌细胞增殖中的后续作用。材料与方法采用UCSC、TCGA和GEPIA数据库分析胃癌组织中snr3c1的表达、预后及免疫浸润情况。采用RT-qPCR、Western blot和免疫荧光检测NR3C1表达、活化、巨噬细胞极化和自噬情况。采用RT-qPCR和ELISA检测IL-10的表达和分泌。用流式细胞术和荧光显微镜分析活性氧（ROS）的产生。Western blot、流式细胞术和功能分析也评估了细胞凋亡、增殖和迁移的变化。幽门螺杆菌感染诱导巨噬细胞中NR3C1的上调和激活。幽门螺杆菌通过调节NR3C1信号通路，促进免疫抑制表型，触发巨噬细胞自噬损伤。巨噬细胞中NR3C1的存在增强了对幽门螺杆菌诱导的免疫抑制微环境的主动反应。这导致胃癌细胞（HGC-27）活性增加，包括增殖、迁移增强、凋亡减少和ROS生成升高。幽门螺杆菌通过NR3C1调控巨噬细胞的免疫抑制微环境，促进胃癌细胞的恶性表型，提示幽门螺杆菌相关胃癌治疗的潜在治疗靶点。

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Helicobacter pylori modulates macrophage polarization via the glucocorticoid receptor to promote gastric cancer cell proliferation

Background

Helicobacter pylori (H. pylori) is recognized as a major risk factor for gastric cancer (GC). However, the precise mechanism by which H. pylori influences macrophage immune responses in cancer progression remains poorly understood. This study investigates how H. pylori affects macrophage polarization via the glucocorticoid receptor (NR3C1) and its subsequent role in gastric cancer cell proliferation.

Materials and methods

NR3C1 expression, prognosis, and immune infiltration in gastric cancer were analyzed using the UCSC, TCGA, and GEPIA databases. NR3C1 expression, activation, macrophage polarization, and autophagy were assessed using RT-qPCR, Western blot, and immunofluorescence. IL-10 expression and secretion were quantified using RT-qPCR and ELISA. Reactive oxygen species (ROS) production was analyzed using flow cytometry and fluorescence microscopy. Western blot, flow cytometry, and functional assays also evaluated apoptosis, proliferation, and migration alterations.

Results

H. pylori infection induces the upregulation and activation of NR3C1 in macrophages. By modulating NR3C1 signaling, H. pylori promotes the immunosuppressive phenotype and triggers macrophage autophagy impairment. NR3C1 presence in macrophages enhances the active response to the H. pylori-induced immunosuppressive microenvironment. This leads to increased activity in gastric cancer cells (HGC-27), including enhanced proliferation, migration, reduced apoptosis, and elevated ROS production.

Conclusion

H. pylori orchestrates the immunosuppressive microenvironment of macrophages via NR3C1, promoting a malignant phenotype in gastric cancer cells and suggesting potential therapeutic targets for H. pylori-related gastric cancer treatment.

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来源期刊

Tissue & cell 医学-解剖学与形态学

CiteScore

3.90

自引率

0.00%

发文量

234

期刊介绍： Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed. Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.