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作 者:关昊[1] 李宗禹 赖婧玥 马建仓[1] GUAN Hao;LI Zongyu;LAI Jingyue;MA Jiancang(Department of Vascular Surgery,Second Affiliated Hospital of Xi'an Jiaotong University,Xi'an 710004,China)
机构地区:[1]西安交通大学第二附属医院血管外科,陕西西安710004
出 处:《药物生物技术》2024年第6期619-623,共5页Pharmaceutical Biotechnology
基 金:陕西省自然科学基础研究计划基金项目(No.2020JQ-555)。
摘 要:本研究旨在探讨益母草碱对胃癌细胞CRL-5822的抑制作用及其潜在分子机制,为其作为胃癌治疗的潜在药物提供理论依据。通过体外实验,评估益母草碱对胃癌细胞增殖、迁移和侵袭的影响,并使用正常胃上皮细胞作为对照。采用分子生物学技术分析PI3K/Akt/GSK-3β信号通路中关键蛋白的磷酸化水平变化,研究其对胃癌细胞恶性生物学行为的调控作用。益母草碱显著抑制了胃癌细胞的增殖、迁移和侵袭能力,且对正常胃上皮细胞的毒性作用较小。分子机制研究表明,益母草碱通过下调PI3K/Akt/GSK-3β信号通路中关键蛋白的磷酸化水平,阻断该信号通路的活性,从而有效抑制胃癌细胞的恶性生物学行为。益母草碱通过调节PI3K/Akt/GSK-3β信号通路抑制胃癌细胞的恶性生物学行为,其特异性抗癌作用为胃癌的治疗提供了实验依据,具有潜在的临床应用价值。This study aims to investigate the inhibitory effects of leonurine on gastric cancer(GC)cells(CRL-5822)and its underlying molecular mechanisms,providing a theoretical basis for its potential application as a therapeutic agent for GC.In vitro experiments were conducted to evaluate the effects of leonurine on the proliferation,migration,and invasion of GC cells,with normal gastric epithelial cells serving as controls.Molecular biology techniques were used to analyze changes in the phosphorylation levels of key proteins in the PI3K/Akt/GSK-3βsignaling pathway to explore its role in regulating the malignant behaviors of GC cells.Leonurine significantly inhibited the proliferation,migration,and invasion of GC cells while exhibiting minimal cytotoxicity toward normal gastric epithelial cells.Mechanistic studies revealed that leonurine downregulated the phosphorylation levels of key proteins in the PI3K/Akt/CSK-3βsignaling pathway,thereby blocking its activity and effectively suppressing the malignant biological behaviors of CC cells.Leonurine inhibits the malignant behaviors of GC cells by modulating the PI3K/Akt/GSK-3βsignaling pathway.Its selective anticancer effects provide valuable experimental evidence for its potential clinical application as a therapeutic agent for gastric cancer.
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