We found that the acquired resistance to GEM or PTX induced the overexpression of OGT in human UCB cell lines, and loss-of-function experiments verified that eliminating OGT function restored chemosensitivity to GEM or PTX, which suggests that O-GlcNAcylation by OGT in UCB contributes to the MDR and cancer aggression through direct or indirect impacts on various oncogenic mechanisms, although the detailed targeted proteins and mode of action remain to be further characterized (Figure 6). Here, OGT is linked to cancer.