Related Experiment Video
Updated: Apr 18, 2026
Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
The non glycanated endocan polypeptide slows tumor growth by inducing stromal inflammatory reaction
Hanane Yassine1,2,3,4, Nathalie De Freitas Caires1,2,3,4,5, Florence Depontieu1,2,3
1Institut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France.
Abstract:
Endocan expression is increasingly studied in various human cancers. Experimental evidence showed that human endocan, through its glycan chain, is implicated in various processes of tumor growth. We functionally characterize mouse endocan which is also a chondroitin sulfate proteoglycan but much less glycanated than human endocan. Distant domains from the O-glycanation site, located within exons 1 and 2 determine the glycanation pattern of endocan. In opposite to the human homologue, overexpression of mouse endocan in HT-29 cells delayed the tumor appearance and reduced the tumor growth rate. This tumor growth inhibition is supported by non glycanated form of mouse endocan. Non glycanated human endocan overexpressed in HT-29, A549 or K1000 cells also exhibited an anti-tumor effect. Moreover, systemic delivery of non glycanated human endocan also results in HT-29 tumor growth delay. In vitro, endocan polypeptide did not affect HT-29 cell proliferation, nor cell viability. In tumor tissue sections, a stromal inflammatory reaction was observed only in tumors overexpressing endocan polypeptide, and depletion of CD122+ cells was able to delete partially the anti-tumor effect of endocan polypeptide. These results reveal a novel pathway for endocan in the control of tumor growth, which involves inflammatory cells of the innate immunity.
Insights
Mouse and human endocan, a proteoglycan, show anti-tumor effects, particularly in non-glycanated forms. This novel pathway involves inflammatory cells, revealing new cancer growth control mechanisms.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Endocan (ESM-1) expression is linked to human cancer progression.
- Its glycan chain is implicated in tumor growth processes.
- Mouse endocan differs from human endocan in glycanation levels.
Purpose of the Study:
- To functionally characterize mouse endocan.
- To investigate the anti-tumor effects of non-glycanated endocan.
- To elucidate the role of endocan in tumor growth control.
Main Methods:
- Overexpression of mouse and human endocan in cancer cell lines (HT-29, A549, K1000).
- Assessment of tumor appearance and growth rate in vivo.
- In vitro proliferation and viability assays.
- Analysis of stromal inflammatory reaction and immune cell involvement (CD122+ cells).
Main Results:
- Overexpression of mouse endocan delayed tumor appearance and reduced growth rate.
- Non-glycanated forms of both mouse and human endocan demonstrated anti-tumor effects.
- Systemic delivery of non-glycanated human endocan also delayed tumor growth.
- Endocan polypeptide alone did not affect cancer cell proliferation or viability.
- Tumors overexpressing endocan polypeptide showed a stromal inflammatory reaction involving CD122+ cells.
Conclusions:
- Mouse endocan, despite lower glycanation, exhibits anti-tumor properties.
- Non-glycanated endocan (human and mouse) possesses significant anti-tumor activity.
- Endocan's anti-tumor effect is mediated through innate immune cells, specifically CD122+ cells, via a novel pathway.
More Related Videos
Related Concept Videos
02:17The Tumor Microenvironment
01:27Tumor Immunotherapy