Tissue & cell · 2025
Helicobacter pylori modulates macrophage polarization via the glucocorticoid receptor to promote gastric cancer cell proliferation.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Xiuping, Weng Yiwei, Yao Yongliang, Shao Shihe, Mao Lingxiang, Wang Jianjun
Аннотация
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.
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.