O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review)
Issued Date
2025-10-01
Resource Type
ISSN
1021335X
eISSN
17912431
Scopus ID
2-s2.0-105010836586
Journal Title
Oncology Reports
Volume
54
Issue
4
Rights Holder(s)
SCOPUS
Bibliographic Citation
Oncology Reports Vol.54 No.4 (2025)
Suggested Citation
Charoensuksai P., Jirawatnotai S. O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review). Oncology Reports Vol.54 No.4 (2025). doi:10.3892/or.2025.8952 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/111369
Title
O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review)
Author(s)
Author's Affiliation
Corresponding Author(s)
Other Contributor(s)
Abstract
Aberrant O‑GlcNAcylation and the upregula‑ tion of O‑GlcNAc transferase (OGT) are key contributors to cancer pathogenesis and progression, driving hyperp‑ roliferative states and metastatic phenotypes. Targeting OGT may suppress cancer progression, positioning OGT and O‑GlcNAc signaling as compelling targets in cancer research. Cholangiocarcinoma (CCA), a rare yet highly aggressive malignancy of the bile duct system, represents a clinical challenge, underscored by its rising global mortality, poor survival outcomes and high recurrence rate, despite advances in awareness, diagnostics and therapeutic strate‑ gies. Consequently, there is need for novel therapeutic modalities. Hyperactive O‑GlcNAcylation and upregulation of OGT are observed in CCA, therefore, targeting protein O‑GlcNAcylation may have clinical potential. The present review aimed to summarize the impact of O‑GlcNAcylation on CCA and CCA‑relevant hallmarks of cancer including cell proliferation, metastasis, metabolic reprogramming, angiogenesis, programmed cell death and tumor‑associated inflammation. 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.