OGT (O-linked N-acetylglucosamine (GlcNAc) transferase)

In vivo, Z-GS significantly inhibited TNBC xenograft growth without detectable toxicity. Z-GS functions as a novel late-stage autophagy inhibitor and exhibits selective anti-TNBC activity, bridging natural product pharmacology and cancer treatment.

Specifically, OGT downregulated several ribosomal proteins, and OGT knockdown influenced proteins across the identified pathways. Taken together, these findings demonstrate that reducing OGT and protein O-GlcNAcylation may enhance the sensitivity of CRC cells to OXA, and the altered pathways may offer new insights into potential mechanisms for overcoming CRC chemoresistance.

By using the hepatocarcinoma cell line Hep3B, we show thanks to two series of deletion mutants that both enzymes preferentially interact via their respective N-terminal regions. Analysis of the O-GlcNAc status of the various FASN deletion mutants shows that stronger interaction with OGT correlates with higher glycosylation, suggesting that OGT catalyzes the transfer of GlcNAc with limited substrate specificity.

In conclusion, this study reveals a novel mechanism by which lidocaine inhibits HER2-positive breast cancer cell proliferation by targeting the OGT-CCNL1 axis, highlighting a potential therapeutic avenue for HER2-positive breast cancer.

The emergence of 5-fluorouracil (5FU) resistance critically compromises chemotherapy efficacy in colorectal cancer (CRC)...Critically, elevated OGT in 5FU-resistant cells drives hyper-O-GlcNAcylation of Erbin at Thr1070, which facilitates its ubiquitin-dependent degradation, alleviating HR suppression to sustain chemoresistance. This defines the OGT-Erbin-HR axis as a central driver of 5FU resistance, proposing therapeutic targeting of this pathway to overcome CRC chemoresistance.

Our findings reveal cross-talk between the HBP, steroid hormone pathway, and tumor immune evasion, and suggest potential strategies for sensitizing UCEC to immunotherapy.

To date, no patients with OGT-CDGs have been reported with hepatoblastoma or other malignancies. Although the occurrence of hepatoblastoma in the proband might be coincidental, the role of O-GlcNAcylation in cancer suggests that the deficiency of OGT activity might be associated with increased cancer risk.

Thus, our findings elucidate the critical role of HCF-1 and O-GlcNAcylation in lung cancer pathogenesis. These insights not only deepen our understanding of lung cancer pathogenesis but also identify potential molecular targets for studies aimed at intervention.

Further study revealed that PET inactivated NF‑κB by down-regulating OGT in BV2 cells, indicating that the protective effect of PET against LPS-induced retinal microglia inflammatory response was achieved by regulating OGT/NF-κB/LCN2 axis. Our findings may contribute to the potential clinical use of PET in treating DR and suggest OGT/NF-κB/LCN2 axis may be the potential therapeutic target of this disease.

Finally, activation of Wnt pathway by LiCl treatment recovered the proliferation and migration of PCa cells repressed by OGT silencing. In conclusion, the present study indicated that OGT-induced O-GlcNAcylation of OR51F2 accelerated PCa progression via activating the Wnt/β-catenin pathway.

In areas where direct evidence in CCA is limited, insights from other gastrointestinal tract cancers may identify potential mechanistic connections, offering a broader context to guide future investigation. Furthermore, the viability of OGT and O‑GlcNAcylation as therapeutic targets is discussed.

GlMYB4, as one of the most strongly induced high temperature-associated genes, showed transactivation activity, and the C-terminal was critical for the transactivation activity. By yeast two-hybrid screening, GlMYB4 may interact with three candidate proteins: calcineurin subunit B (CNB), O-linked N-acetylglucosamine transferase (OGT), and cleavage and polyadenylation specificity factor (CPSF) to modulate high temperature tolerance.