ArticleBMC cancer2018
Suppressed OGT expression inhibits cell proliferation while inducing cell apoptosis in bladder cancer.
Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Glycosylation as a dynamic regulator of RLR and cGAS-STING innate immune signalling pathways.Communications biology · 2026Review
- Reducing OGT and O-GlcNAcylation enhance the anticancer effects of oxaliplatin in SW620 metastatic colorectal cancer cells.PloS one · 2026Article
- O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review).Oncology reports · 2025Review
- Integrated in vivo functional screens and multiomics analyses identify α-2,3-sialylation as essential for melanoma maintenance.Science advances · 2025Article
- Immune cell metabolism in cancer drug resistance: Advances in target discovery and clinical translation.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- The post-translational modification O-GlcNAc is a sensor and regulator of metabolism.Open biology · 2024Review
- The roles of OGT and its mechanisms in cancer.Cell & bioscience · 2024Review
- Knockdown of ZNF280A inhibits cell proliferation and promotes cell apoptosis of bladder cancer.Histology and histopathology · 2024Article
- Identification and verification of anoikis-related gene markers to predict the prognosis of patients with bladder cancer and assist in the diagnosis and treatment of bladder cancer.Translational cancer research · 2024Article
- Tumor glucose metabolism and the T cell glycocalyx: implication for T cell function.Frontiers in immunology · 2024Review
- Altered Glycosylation in Progression and Management of Bladder Cancer.Molecules (Basel, Switzerland) · 2023Review
- Insight into autophagy in platinum resistance of cancer.International journal of clinical oncology · 2023Review
- OGT controls mammalian cell viability by regulating the proteasome/mTOR/ mitochondrial axis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- O-GlcNAcylation: an important post-translational modification and a potential therapeutic target for cancer therapy.Molecular medicine (Cambridge, Mass.) · 2022Review
- O-GlcNAc Transferase (OGT) Protects Cerebral Neurons from Death During Ischemia/Reperfusion (I/R) Injury by Modulating Drp1 in Mice.Neuromolecular medicine · 2022Article
- Article
- Review
- Ogt Demonstrated Conspicuous Clinical Significance in Cancers, from Pan-Cancer to Small-Cell Lung Cancer.Journal of oncology · 2022Article
- Inhibition of O-GlcNAc transferase sensitizes prostate cancer cells to docetaxel.Frontiers in oncology · 2022Article
- TargetingFrontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThis study aimed to explore hyper-O-linked N-acetylglucosaminylation (O-GlcNAcylation) with an elevation of the expression of O-linked-β-N-acetylglucosamine transferase (OGT) in human bladder cancer.
methodsImmunohistochemical staining for OGT and O-GlcNAcylation was performed in 20 paired human bladder cancer and adjacent normal tissues, as well as in human bladder cancer tissue microarrays (N = 169). The expression level of OGT and O-GlcNAcylation in cell lines were detected using the Western blot analysis. The effects of O-GlcNAcylation on the cell proliferation of bladder cancer were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and clone formation assays. Cell apoptosis and cell cycle analysis were detected using flow cytometry. The autophagy of bladder cancer cells was investigated using the Western blot analysis, and GFP-LC3 plasmid was used to detect the autophagic flux. MTT assay was performed to detect the sensitivity of bladder cancer cells to cisplatin after OGT knockdown.
resultsThe expression of OGT and the O-GlcNAcylation were upregulated in bladder cancer tissues and cell lines. O-GlcNAcylation and OGT were observed in nucleus and cytoplasm and found to be higher in muscle-invasive bladder cancer (MIBC) than in non-muscle-invasive bladder cancer (NMIBC). Reducing hyper-O-GlcNAcylation by OGT knockdown inhibited the proliferation of bladder cancer cells in vitro and xenograft tumor growth in vivo, triggered apoptosis, as well as led to cell cycle arrest. It also increased autophagy in bladder cancer cells. This study demonstrated increased autophagy pro-survival, but not pro-death. Reducing hyper-O-GlcNAcylation by OGT knockdown facilitated the chemosensitivity of bladder cancer cells to cis-platinum.
conclusionsThe data indicated that hyper-O-GlcNAcylation enhanced oncogenic phenotypes and was involved in DNA damage response in bladder cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.