Title:TROP2 Down-regulated DSG2 to Promote Gastric Cancer Cell Invasion
and Migration by EGFR/AKT and DSG2/PG/β-Catenin Pathways
Volume: 22
Issue: 8
关键词:
TROP2、DSG2、胃癌、桥粒、粘附、相互作用蛋白。
摘要:
Background: 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.
Aims and Objective: 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.
Method: 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.
Result: 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.
Conclusion: TROP2 promotes cell invasion and migration in gastric cancer by decreasing DSG2 expression
through EGFR/AKT and DSG2/PG/β-catenin pathways.
