Actinidia chinensis polysaccharide interferes with the epithelial-mesenchymal transition of gastric cancer by regulating the nuclear transcription factor-κB pathway to inhibit invasion and metastasis.

Zhang Guangshun, X U Xiaonan, X U Chuyun, Liao Guanghui, X U Hao, Lou Zhaohuan, Zhang Guangji
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Abstract

Objective: To investigate the mechanisms of the effect of Actinidia chinensis polysaccharide (ACPS) on the invasion and metastasis of gastric cancer cells.

Methods: BGC-823-Luc gastric cancer cells stably transfected with a luciferase gene were used to establish an insitutransplanted tumor mouse model. A live mouse imaging system was used to observe tumor growth, and hematoxylin and eosin staining was applied to analyze tissue histopathology. Transwell and scratch wound assays were performed to examine the invasive and migratory ability of BGC-823 cells. Immunofluorescence, confocal microscopy, immunohistochemistry, and Western blot assays were used to analyze the expressions of the nuclear transcription factor-κB (NF-κB) signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins.

Results: ACPS significantly inhibited the growth of subcutaneously transplanted BGC-823-Luc gastric cancer tumors in nude mice and reduced inflammatory cell infiltration in tumor tissues. ACPS inhibited Epidermal Growth Factor-induced invasion, migration, and morphological changes in the cytoskeleton of BGC-823 cells. ACPS inhibited gastric cancer EMT and decreased the expression of matrix metallopeptidase 9, N-cadherin and p-NF-κB p65 in transplanted tumor tissues. ACPS inhibited the expression of matrix metalloproteinases and vascular adhesion factors in BGC-823 cells, promoted p65-NF-κB nuclear translocation, and regulated proteins associated with the NF-κB p65 pathway.

Conclusions: ACPS inhibited gastric cancer invasion and metastasis both in vivo and in vitro, which evidenced the inhibition of gastric cancer EMT viaregulating the NF-κB inflammatory pathway.

放线菌多糖通过调节核转录因子-κB通路干扰胃癌的上皮-间质转化,从而抑制侵袭和转移。
目的:研究放线菌多糖(ACPS)对胃癌细胞侵袭和转移的影响机制:研究放线菌多糖(ACPS)对胃癌细胞侵袭和转移的影响机制:方法:用稳定转染荧光素酶基因的BGC-823-Luc胃癌细胞建立体内移植肿瘤小鼠模型。活体小鼠成像系统用于观察肿瘤生长,苏木精和伊红染色用于分析组织病理学。透孔试验和划痕伤口试验用于检测 BGC-823 细胞的侵袭和迁移能力。免疫荧光、共聚焦显微镜、免疫组织化学和 Western 印迹分析用于分析核转录因子-κB(NF-κB)信号通路和上皮-间质转化(EMT)相关蛋白的表达:结果:ACPS能明显抑制裸鼠皮下移植的BGC-823-Luc胃癌肿瘤的生长,并减少肿瘤组织中的炎症细胞浸润。ACPS 可抑制表皮生长因子诱导的 BGC-823 细胞的侵袭、迁移和细胞骨架的形态变化。ACPS 可抑制胃癌的 EMT,降低移植肿瘤组织中基质金属肽酶 9、N-cadherin 和 p-NF-κB p65 的表达。ACPS 可抑制 BGC-823 细胞中基质金属蛋白酶和血管粘附因子的表达,促进 p65-NF-κB 核转位,并调节与 NF-κB p65 通路相关的蛋白:结论:ACPS可抑制胃癌的体内和体外侵袭和转移,证明其可通过调节NF-κB炎症通路抑制胃癌的EMT。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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