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TROP2 Down-regulated DSG2 to Promote Gastric Cancer Cell Invasion and Migration by EGFR/AKT and DSG2/PG/β-Catenin Pathways.

Author information

Affiliations

  • 1. Key Laboratory of Antibody Technique of National Health Commission, Nanjing Medical University, Nanjing 211166, China.
      Authors
    • Yang T 1
    • Bian S 1
    • Chang X 1
    • Zhang Q 1
    • Tang Q 1
    • Feng Z 1, 2
    (6 authors)
  • 2. Jiangsu Key Lab. of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing 211166, China.
      Authors
    • Jia L 2
    • Feng Z 1, 2
    (2 authors)
  • 3. Cancer Center, Bayannur Hospital, Bayannur, Inner Mongolia 015000, China.
      Authors
    • Zhu J 3
    • Yang Z 3
    (2 authors)

ORCIDs linked to this article

Current Cancer Drug Targets, 01 Aug 2022, 22(8):691-702
https://doi.org/10.2174/1568009622666220407111013 PMID: 35392784 

Abstract 

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.

Full text links 

Read article at publisher's site: https://doi.org/10.2174/1568009622666220407111013

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Funding 

Funders who supported this work.

NSFC, Natural Science Foundation of China (1)