The non glycanated endocan polypeptide slows tumor growth by inducing stromal inflammatory reaction
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Hanane Yassine1,2,3,4,*, Nathalie De Freitas Caires1,2,3,4,5,*, Florence Depontieu1,2,3, Arnaud Scherpereel1,2,3,4,6, Ali Awad1,2,3,4, Anne Tsicopoulos1,2,3,4, Christophe Leboeuf7, Anne Janin7, Catherine Duez1,2,3,4, Bogdan Grigoriu1,2,4,8,9, Philippe Lassalle1,2,3,4
1 Institut Pasteur de Lille, Center for Infection and Immunity of Lille, Lille, France
2 Univ Lille Nord de France, Lille, France
3 CNRS, UMR 8204, Lille, France
4 Institut National de la Santé et de la Recherche Médicale, Lille, France
5 Lunginnov, Lille, France
6 CHRU Lille, Hôpital Calmette, Lille, France
7 Institut National de la Santé et de la Recherche Médicale, Paris, France
8 Regional Institute of Oncology, Iasi, Romania
9 University of Medicine and Pharmacy “Gr.T.Popa” Iasi, Iasi, Romania
* These authors contributed equally to this work
Philippe Lassalle, email:
Keywords: Mouse; Endocan; Glycosaminoglycan; Tumor; Leukocytes.
Received: September 22, 2014 Accepted: October 21, 2014 Published: October 21, 2014
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.
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