ArticlePloS one2013
N-linked glycosylation supports cross-talk between receptor tyrosine kinases and androgen receptor.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Meta-analysis of prostate cancer gene expression data identifies a novel discriminatory signature enriched for glycosylating enzymes.BMC medical genomics · 2014Pooled it
- Aberrations in the glycosylation of receptor tyrosine kinases: A focus on lung adenocarcinoma.CytoJournal · 2025Review
- Impaired myoblast differentiation and muscle IGF-1 receptor signaling pathway activation after N-glycosylation inhibition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Castration-resistant prostate cancer cells are dependent on the high activity of CDK7.Journal of cancer research and clinical oncology · 2023Article
- O-GlcNAc transferase maintains metabolic homeostasis in response to CDK9 inhibition.Glycobiology · 2022Article
- O-GlcNAc transferase couples MRE11 to transcriptionally active chromatin to suppress DNA damage.Journal of biomedical science · 2022Article
- Article
- Role of Glycans on Key Cell Surface Receptors That Regulate Cell Proliferation and Cell Death.Cells · 2021Review
- Glutaminolysis is a metabolic route essential for survival and growth of prostate cancer cells and a target of 5α-dihydrotestosterone regulation.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- New strategies to treat AML: novel insights into AML survival pathways and combination therapies.Leukemia · 2021Review
- Fucosyltransferase 8 modulates receptor tyrosine kinase activation and temozolomide resistance in glioblastoma cells.American journal of cancer research · 2021Article
- Relative Quantification of Phosphorylated and Glycosylated Peptides from the Same Sample Using Isobaric Chemical Labelling with a Two-Step Enrichment Strategy.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Article
- Oligosaccharyltransferase Inhibition Reduces Receptor Tyrosine Kinase Activation and Enhances Glioma Radiosensitivity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- High OGT activity is essential for MYC-driven proliferation of prostate cancer cells.Theranostics · 2019Article
- Prostate Cancer Energetics and Biosynthesis.Advances in experimental medicine and biology · 2019Review
- Delineation of the androgen-regulated signaling pathways in prostate cancer facilitates the development of novel therapeutic approaches.Current opinion in pharmacology · 2018Review
- Role of IGF-1R in ameliorating apoptosis of GNE deficient cells.Scientific reports · 2018Article
- Inhibition of the Hexosamine Biosynthetic Pathway by targeting PGM3 causes breast cancer growth arrest and apoptosis.Cell death & disease · 2018Article
- Glycosylation as a Main Regulator of Growth and Death Factor Receptors Signaling.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is the second most common cause of cancer-associated deaths in men and signalling via a transcription factor called androgen receptor (AR) is an important driver of the disease. Androgen treatment is known to affect the expression and activity of other oncogenes including receptor tyrosine kinases (RTKs). In this study we report that AR-positive prostate cancer cell-lines express 50% higher levels of enzymes in the hexosamine biosynthesis pathway (HBP) than AR-negative prostate cell-lines. HBP produces hexosamines that are used by endoplasmic reticulum and golgi enzymes to glycosylate proteins targeted to plasma-membrane and secretion. Inhibition of O-linked glycosylation by ST045849 or N-linked glycosylation with tunicamycin decreased cell viability by 20%. In addition, tunicamycin inhibited the androgen-induced expression of AR target genes KLK3 and CaMKK2 by 50%. RTKs have been shown to enhance AR activity and we used an antibody array to identify changes in the phosphorylation status of RTKs in response to androgen stimulation. Hormone treatment increased the activity of Insulin like Growth Factor 1-Receptor (IGF-1R) ten-fold and this was associated with a concomitant increase in the N-linked glycosylation of the receptor, analyzed by lectin enrichment experiments. Glycosylation is known to be important for the processing and stability of RTKs. Inhibition of N-linked glycosylation resulted in accumulation of IGF-1R pro-receptor with altered mobility as shown by immunoprecipitation. Confocal imaging revealed that androgen induced plasma-membrane localization of IGF-1R was blocked by tunicamycin. In conclusion we have established that the glycosylation of IGF-1R is necessary for the full activation of the receptor in response to androgen treatment and that perturbing this process can break the feedback loop between AR and IGF-1R activation in prostate cells. Achieving similar results selectively in a clinical setting will be an important challenge in the future.
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Registered trials
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