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文章编号:1672-6987(2026)02-0024-09;DOI:10. 16351/j. 1672-6987. 2026. 02. 004
薄思佳 1 ,王吉龙 2 ,隋 磊 2 ,郭传龙 3 ,赵睿汝 4 ,朱 婷 2 ,房瑶瑶 5 ,宋海平 2 ,栾朝辉 2 , 王成双 2 ,孙 丽 2* (1. 山东第二医科大学 临床医学院,山东 潍坊 261053;2. 康复大学 青岛中心医院,山东 青岛 266042;3. 青岛科技大学 化工学院,山东 青岛 266042;4. 南昌大学 玛丽女王学院,江西 南昌 330031;5. 海南医科大学,海南 海口 571199)
摘 要:通过网络药理学和实验验证研究柳穿鱼黄素对宫颈癌HeLa和SiHa细胞增殖和迁移的影 响。首先通过 PharmMapper和 SwissTargetPrediction数据库预测柳穿鱼黄素作用靶点,然后与来 自GeneCards和OMIM等多个数据库的宫颈癌(CC)的疾病靶点进行交集分析,初步确定柳穿鱼黄 素在CC治疗中的潜在作用靶点,进而构建靶蛋白相互作用网络,并依托基因本体论(GO)与京都基 因和基因组百科全书(KEGG)筛选柳穿鱼黄素作用于CC的可能信号通路。以HeLa/SiHa细胞为 模型,采用CCK-8、划痕、Transwell、集落形成和Western blotting等多种实验,研究柳穿鱼黄素对细 胞增殖、迁移、克隆及 JAK2/STAT3表达的作用。结果 KEGG 分析表明,柳穿鱼黄素作用于 CC 显著富集信号通路以 Pathways in cancer、JAK2/STAT3 通路、PI3K/Akt 等为主。细胞实验结 果显示,柳穿鱼黄素可显著抑制宫颈癌 HeLa 和 SiHa 细胞增殖和迁移的能力,且具有浓度依赖 性(P<0. 01),同时柳穿鱼黄素可降低宫颈癌HeLa和SiHa细胞p-JAK2和p-STAT3蛋白的表达水 平(P<0. 01)。柳穿鱼黄素可能通过调节JAK2/STAT3信号通路抑制宫颈癌细胞的增殖与迁移。
关键词:柳穿鱼黄素;宫颈癌;网络药理学;增殖;迁移
中图分类号:R 71 文献标志码:A
引用格式:薄思佳,王吉龙,隋磊,等 . 柳穿鱼黄素通过调节 STAT3 通路抑制宫颈癌细胞的 增殖与迁移[J]. 青岛科技大学学报(自然科学版),2026,47(2):24-32.
BO Sijia, WANG Jilong, SUI Lei, et al. Pectolinarigenin inhibits the proliferation and migration of cervical cancer cells by regulating the STAT3 signaling pathway[J]. Journal of Qingdao University of Science and Technology(Natural Science Edition),2026,47(2):24-32.
Pectolinarigenin Inhibits the Proliferation and Migration of Cervical Cancer Cells by Regulating the STAT3 Signaling Pathway
BO Sijia1 ,WANG Jilong2 ,SUI Lei2 ,GUO Chuanlong3 ,ZHAO Ruiru4 ,ZHU Ting2 ,FANG Yaoyao5 , SONG Haiping2 ,LUAN Zhaohui2 ,WANG Chengshuang2 ,SUN Li2 (1. School of Clinical Medicine, Shandong Second Medical University,Weifang 261053,China;2. Qingdao Central Hospital, University of Health and Rehabilitation Sciences,Qingdao 266042,China;3. College of Chemical Engineering,Qingdao University of Science and Technology,Qingdao 266042,China;4. Queen Mary College of Nanchang University,Nanchang 330031,China;5. Hainan Medical University,Haikou 571199,China)
Abstract:To investigate the effects of pectolinarigenin on the proliferation and migration of cervical cancer HeLa and SiHa cells through network pharmacology and experimental verification. The targets of pectolinarigenin were screened using the PharmMapper and SwissTargetPrediction databases. Disease-related targets associated with cervical cancer (CC) were obtained from multiple databases including GeneCards and OMIM. After intersection analysis, a protein-protein interaction (PPI) network was constructed to screen key targets. Pathway enrichment analysis was performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). This study investigated the effects of linarin on the viability, migration, clonogenicity, and JAK2/STAT3 expression in HeLa/SiHa cells using a series of assays including CCK-8, wound healing, Transwell, colony formation, and Western blotting. Results KEGG analysis based on database retrieval showed that the most significant signaling pathways mainly included "Pathways in cancer",JAK2/STAT3 pathway and PI3K/Akt path⁃ way. Pectolinarigenin inhibited the proliferation and migration of cervical cancer HeLa and SiHa cells in a concentration-dependent manner (P<0. 01), and it also reduced the protein expression levels of phosphorylated JAK2(p-JAK2) and phosphorylated STAT3(p-STAT3)(P<0. 01). Pectolinarigenin may inhibit the proliferation and migration of cervical cancer cells by regulating the JAK2/STAT3 signaling pathway.
Key words:pectolinarigenin; cervical cancer; network pharmacology; proliferation; migration
收稿日期:2025-10-24
基金项目:山东省医学会科研项目重点项目(YXH2024ZM003);青岛市医药卫生科研计划项目(2021-WJZD095);山东省医药卫生科技 发展计划项目(2016WS0562);山东省重点研发计划项目(2018GSF118238).
作者简介:薄思佳(2000—),女,硕士研究生 . * 通信联系人 .