Abstract
Abstract Question We recently introduced the carbohydrate-binding protein Galectin-1 (Gal-1) as a novel tolerogeneic molecule in neuroblastoma (NB). NB-secreted Gal-1 suppressed the maturation of dendritic cells (DC) and inhibited T cell function. Here, we focused on the question whether tumor-derived Gal-1 is the decisive factor to promote tumor growth in our model for NB. Methods C57Bl/6J-derived orthotopic growing NB cells (named NB975A) were used for all culture as well in vivo experiments. Gal-1 knock-down clones (GL) were generated by stable transfection of wt NB975A cells (NBA) with the antisense Gal-1 expression vector (NBA-GL), (kindly provided by Dr. Rabinovich). Blasticidine resistant (5 mikrogram/ml) transfectants were cloned by limited dilution. Protein expression of Gal-1 was determined by Western blot. Orthotopic NB tumors were generated in C57Bl/6J wild type and Gal-1-knock-out (Lgals-/-) female mice by subcapsular tumor cell injection of NBA-GL or wild type NBA (1x106, 0,1 ml PBS) into the left kidney. Primary tumor growth was analyzed by using high frequency ultrasound measurement. Mice were sacrificed 23 days after tumor inoculation and tumor tissue was harvested for further analysis. Results NBA-GL showed 50% reduced protein expression of Gal-1 compared to control wild type NBA cells. In vitro viability and proliferation of the tumor cells was not affected by the transfection. Mice inoculated with NBA-GL cells had significantly smaller primary tumors when compared with control animals that received the NBA cells. Gal-1 sufficient tumor cells injected in Gal-1-deficient host mice grew normally. Conclusion Tumor-derived Gal-1 and not its expression in host is critical for the promotion of tumor growth. Citation Format: Stefan Fest. Tumor-derived Galectin-1 promotes tumor growth in an orthotopic C57Bl/6 NB mouse model [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4559.
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