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当代肿瘤药物靶点

Editor-in-Chief

ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

General Research Article

TROP2 下调 DSG2 通过 EGFR/AKT 和 DSG2/PG/β-Catenin 通路促进胃癌细胞侵袭和迁移

卷 22, 期 8, 2022

发表于: 09 June, 2022

页: [691 - 702] 页: 12

弟呕挨: 10.2174/1568009622666220407111013

价格: $65

摘要

背景:胃癌(GC)是全球第四大常见癌症,也是癌症相关死亡的第二大原因。 TROP2 过表达与许多癌症密切相关,包括胃肠道肿瘤。 DSG2是细胞粘附中的重要蛋白质,其缺失影响细胞迁移。 目的与目的:本研究旨在探讨TROP2促进胃癌发生的具体机制,为胃癌的防治提供依据。 方法:DSG2通过免疫共沉淀和质谱鉴定为GC细胞中TROP2的相互作用蛋白。用 TROP2 过压或敲低研究了 TROP2 对 DSG2 表达的调节行为。由 DSG2 介导的细胞 - 细胞粘附能力通过粘附相关测定进行评估。进行电子显微镜观察以访问GC肿瘤桥粒组装。通过蛋白质印迹评估 EGFR/AKT 和 DSG2/PG/β-连环蛋白途径中的蛋白质。 结果:本研究表明, 胃癌细胞中 TROP2 的大量表达降低了 DSG2 水平以及桥粒粘附, 增加了细胞侵袭和迁移, 并通过 EGFR/AKT 和 DSG2/PG/β-catenin 途径促进了恶性进展。 结论:TROP2通过EGFR/AKT和DSG2/PG/β-catenin通路降低DSG2表达,促进胃癌细胞侵袭和迁移。

关键词: TROP2、DSG2、胃癌、桥粒、粘附、相互作用蛋白。

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