Cell cycle regulation in cancer cells by O-GlcNAcylation.

Cancer remains one of the leading causes of death worldwide. Due to the multiple molecular mechanisms involved in cell transformation, its biology continues to be studied from different perspectives and in other research areas. A hallmark of cancer is its accelerated proliferation and overactivation of the cell cycle, caused by a dysregulated metabolism and the activation of different signaling pathways, such as the PI3/K-Akt pathway. On the other hand, the hexosamine biosynthetic pathway plays an essential role in producing UDP-GlcNAc, the primary substrate for O-GlcNAcylation. This non-canonical post-translational modification regulates protein stability, localization and interactions. This work aims to examine the role of the O-GlcNAcylation in regulating the cell cycle across diverse types of cancer and its involvement in the PI3/K-Akt pathway as a promoter of the cell cycle progression. Additionally, the study also proposes new alternatives for cancer diagnosis, prognosis, and treatment.