Cancer cells depend on altered metabolism and nutrient uptake to generate and keep the malignant phenotype. Recent work suggests that the metabolite availability to the hexosamine and Golgi O‐glycosylation pathways exerts control over cell signaling, gene expression and cell migration (Alisson‐Silva etal., Plos One, 8: e60471, 2013). Indeed, high glucose concentration increases O‐glycosylation of FN (onFN), which generates the onfFN, and modulates tumorogenesis. Herein we implicate hiperglycemia in facilitating cancer progression and increasing onFN expression in vivo. Cells from colon carcinoma of C57BL/6 mice (MC‐38 cell line) were subcutaneously inoculated in streptozotocin (STZ)‐treated or untreated C57BL/6 mice. Subcutaneous tumors from STZ‐treated group were higher and more vascularized when compared with vehicle group. Tumors from STZ‐treated mice presented high expression of alpha2‐6‐Neu5Ac and alpha1‐3‐/ alpha1‐6‐Fucose (Fuc) containing glycoconjugates as well as increased expression of onFN. These data suggest that metabolite availability modulates cell surface glycosylation contributing to tumor formation and progression.Grant Funding Source: Supported by CNPq, FAPERJ and CAPES