Abstract：
Gastric cancer (GC) is the fourth most commonly found cancer and the second- highest cause of cancer-related death worldwide. TROP2 overexpression is closely related to many cancers, including gastrointestinal tumors. DSG2 is an important protein in cell adhesion, and its loss affects cell migration.
This study aimed to explore the specific mechanism of TROP2 in promoting gastric cancer and provide a basis for the prevention and treatment of gastric cancer.
DSG2 was identified as an interacting protein of TROP2 in GC cells by coimmunoprecipitation and mass spectrometry. The regulated behavior of TROP2 on DSG2 expression was investigated with TROP2 over-expressure or knockdown. Cell-cell adhesion capacity mediated by DSG2 was evaluated by adhesion-related assays. Electron microscope observation was made for accessing GC tumor desmosome assembly. Proteins in EGFR/AKT and DSG2/PG/β-catenin pathways were evaluated by western blotting.
This study suggests that abundant expression of TROP2 in GC cells lessened DSG2 levels as well as desmosome adhesion, increased cell invasion and migration, and promoted malignant progression through EGFR/AKT and DSG2/PG/β-catenin pathways.
TROP2 promotes cell invasion and migration in gastric cancer by decreasing DSG2 expression through EGFR/AKT and DSG2/PG/β-catenin pathways.
This study aimed to explore the specific mechanism of TROP2 in promoting gastric cancer and provide a basis for the prevention and treatment of gastric cancer.
DSG2 was identified as an interacting protein of TROP2 in GC cells by coimmunoprecipitation and mass spectrometry. The regulated behavior of TROP2 on DSG2 expression was investigated with TROP2 over-expressure or knockdown. Cell-cell adhesion capacity mediated by DSG2 was evaluated by adhesion-related assays. Electron microscope observation was made for accessing GC tumor desmosome assembly. Proteins in EGFR/AKT and DSG2/PG/β-catenin pathways were evaluated by western blotting.
This study suggests that abundant expression of TROP2 in GC cells lessened DSG2 levels as well as desmosome adhesion, increased cell invasion and migration, and promoted malignant progression through EGFR/AKT and DSG2/PG/β-catenin pathways.
TROP2 promotes cell invasion and migration in gastric cancer by decreasing DSG2 expression through EGFR/AKT and DSG2/PG/β-catenin pathways.
摘要：
胃癌（GC）是全球第四大最常见的癌症，也是癌症相关死亡的第二大原因。TROP2过表达与多种癌症密切相关,包括胃肠道肿瘤.DSG2是细胞粘附的重要蛋白,其损失影响细胞迁移。
本研究旨在探讨TROP2促进胃癌的具体机制，为胃癌的防治提供依据。
通过共免疫沉淀和质谱鉴定DSG2是GC细胞中TROP2的相互作用蛋白。用TROP2超压或敲低研究TROP2对DSG2表达的调节行为。通过粘附相关测定评估由DSG2介导的细胞-细胞粘附能力。电镜观察进入GC肿瘤桥粒组装。EGFR/AKT和DSG2/PG/β-catenin途径中的蛋白质通过蛋白质印迹法进行评估。
这项研究表明，TROP2在GC细胞中的大量表达降低了DSG2水平以及桥粒粘附，增加细胞侵袭和迁移，并通过EGFR/AKT和DSG2/PG/β-catenin通路促进恶性进展。
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。
本研究旨在探讨TROP2促进胃癌的具体机制，为胃癌的防治提供依据。
通过共免疫沉淀和质谱鉴定DSG2是GC细胞中TROP2的相互作用蛋白。用TROP2超压或敲低研究TROP2对DSG2表达的调节行为。通过粘附相关测定评估由DSG2介导的细胞-细胞粘附能力。电镜观察进入GC肿瘤桥粒组装。EGFR/AKT和DSG2/PG/β-catenin途径中的蛋白质通过蛋白质印迹法进行评估。
这项研究表明，TROP2在GC细胞中的大量表达降低了DSG2水平以及桥粒粘附，增加细胞侵袭和迁移，并通过EGFR/AKT和DSG2/PG/β-catenin通路促进恶性进展。
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。
