Epithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy, and understanding the molecular changes associated with EOC etiology could lead to the identification of novel targets for more effective therapeutic interventions. Glycosylation represents a post-translational modification (PTM) of proteins playing a major role in various cellular functions. Moreover, glycosylation participates in major pathobiological events during tumor progression, as aberrant expression of glycan structures has been shown to contribute in alterations of specific cellular onco-phenotypes, including tumor cell proliferation, migration and invasion. This review aims to describe what is currently known about aberrant glycosylation in EOC, and more specifically, the contribution of aberrant O-linked glycosylation in EOC progression. We also discuss our findings about the altered GALNT3 overexpression in EOC and its involvement in disease dissemination through aberrant mucin O-glycosylation, as well as the potential to exploit the role of GALNT3 in understanding the general mechanisms of abnormal glycosylation implicated in EOC spreading. Further analyses in cancer glycobiology could significantly enhance our understanding of the molecular mechanisms of cancer progression, including EOC dissemination, and could lead to the identification of novel biomarkers/therapeutic targets for better management of this deadly disease.
Biomedical Reviews 2014; 25: 83-92.
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