Abstract

Abstract Galectins (Gal) belong to a family of endogenous lectins specifically recognizing sugar motives and playing an important role in the biology of tissue repair and cancer. It has been shown that the tandem-repeat lectin Gal-8 plays an essential role in tumor angiogenesis by improving endothelial cell migration and capillary tube formation. Interestingly by a more prominent way than the proangiogenic growth factor VEGF. Thus, new question arises, i.e. does Gal-8 improves endothelial cell proliferation? To provide answer to that question the MTT and BrDu proliferation assays using HUVEC (human umbilical vein endothelial cells) as a model were used. We found that Gal-8 induces cell proliferation in combination with VEGF, but Gal-8 alone does not exhibit any significant effect. Furthermore, we studied whether human Gal-8 induces production of a bioactive extracellular matrix (ECM) scaffold by cancer associated fibroblasts (CAF). In parallel, the effect of Gal-8 on ECM production by human dermal fibroblasts (HDF) was studied as well. Adding Gal-8 to the culture medium led the CAF to generate a very fine structured 3D meshwork especially rich in fibronectin. Contrary, the ECM production by HDF was not that apparent. Since ECM-cell interactions play an important role in the ability of tumors to spread and form metastasis further research focused on roles of the tandem-repeat-type Gal-8 in other steps of tumorigenesis is warranted by present in vitro study. This study was supported in part by the Grant Agency of Ministry of Education, Science, Research, and Sport of the Slovak Republic (VEGA-1/0404/15 and VEGA-1/0048/15) and the Agency for Science and Research under the contract no. APVV-0408-12 and APVV-14-0731. Citation Format: Peter Gal, Lenka Varinska, Martin Kello, Jan Mojzis, Barbora Dvorankova, Karel Smetana Jr.. Galectin-8 favors growth of endothelial cells and induces production of extracellular matrix by cancer associated fibroblasts. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2015 Nov 5-9; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl 2):Abstract nr LB-A23.

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