Related Experiment Videos
CD55 is over-expressed in the tumour environment
1CRC Academic Unit of Clinical Oncology, University of Nottingham, City Hospital, Hucknall Road, Nottingham, NG5 1PB, UK
British Journal of Cancer
|January 5, 2001
Summary
CD55, also known as 791Tgp72, is highly expressed on tumor cells and in the tumor stroma. This increased CD55 expression suggests its potential as a target for cancer imaging and immunotherapy.
Area of Science:
- Immunology
- Oncology
- Cell Biology
Background:
- CD55 (Complement Decay-Accelerating Factor) is a cell surface protein that regulates complement activation.
- The antigen 791Tgp72, a known target for tumor imaging and vaccines, has been identified as CD55.
- Tumor microenvironments exhibit altered protein expression, impacting therapeutic strategies.
Purpose of the Study:
- To quantify CD55 expression in the tumor environment.
- To investigate the source of CD55 in the tumor stroma.
- To evaluate CD55's potential as a therapeutic target.
Main Methods:
- Quantitative analysis of CD55 cell surface expression on tumor cells versus normal cells.
- Immunohistochemical staining of colorectal tumors to assess stromal CD55.
- Measurement of extracellular CD55 deposition by epithelial and endothelial cells.
- Assessment of CD55 expression on HUVEC cells following VEGF exposure.
Main Results:
- Tumor cells displayed a 4-100 fold increase in CD55 cell surface expression compared to normal cells.
- High CD55 expression was observed in the stroma of colorectal tumors.
- Tumor cell lines deposited extracellular CD55 proportional to cell surface expression.
- HUVEC cells produced significant extracellular CD55 despite low cell surface expression, which was further increased by VEGF.
Conclusions:
- CD55 is significantly upregulated on tumor cells and within the tumor stroma.
- Both tumor cells and associated endothelium contribute to stromal CD55.
- The elevated expression of CD55 in the tumor microenvironment supports its utility as a target for cancer imaging and immunotherapy.