The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
O-GlcNAc Transferase Integrates Metabolic Pathways to Regulate the Stability of c-MYC in Human Prostate Cancer Cells
Abstract
Metabolic disruptions that occur widely in cancers offer an attractive focus for generalized treatment strategies. The hexosamine biosynthetic pathway (HBP) senses metabolic status and produces an essential substrate for O-linked β-N-acetylglucosamine transferase (OGT), which glycosylates and thereby modulates the function of its target proteins. Here, we report that the HBP is activated in prostate cancer cells and that OGT is a central regulator of c-Myc stability in this setting. HBP genes were overexpressed in human prostate cancers and androgen regulated in cultured human cancer cell lines. Immunohistochemical analysis of human specimens (n = 1987) established that OGT is upregulated at the protein level and that its expression correlates with high Gleason score, pT and pN stages, and biochemical recurrence. RNA interference–mediated siliencing or pharmacologic inhibition of OGT was sufficient to decrease prostate cancer cell growth. Microarray profiling showed that the principal effects of OGT inhibition in prostate cancer cells were related to cell-cycle progression and DNA replication. In particular, c-MYC was identified as a candidate upstream regulator of OGT target genes and OGT inhibition elicited a dose-dependent decrease in the levels of c-MYC protein but not c-MYC mRNA in cell lines. Supporting this relationship, expression of c-MYC and OGT was tightly correlated in human prostate cancer samples (n = 1306). Our findings identify HBP as a modulator of prostate cancer growth and c-MYC as a key target of OGT function in prostate cancer cells. Cancer Res; 73(16); 5277–87. ©2013 AACR.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources
Huang, D. W., Sherman, B. T., & Lempicki, R. A. (2009) · Nature Protocols · doi:10.1038/nprot.2008.211 · Cited by 35,890
Selective inhibition of BET bromodomains
Filippakopoulos, P., Qi, J., Picaud, S., Shen, Y., Smith, W. B., Fedorov, O., Morse, E. M., Keates, T., Hickman, T. T., Felletar, I., et al. (2010) · Nature · doi:10.1038/nature09504 · Cited by 4,262
Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism
Ying, H., Kimmelman, A. C., Lyssiotis, C. A., Hua, S., Chu, G. C., Fletcher-Sananikone, E., Locasale, J. W., Son, J., Zhang, H., Coloff, J. L., et al. (2012) · Cell · doi:10.1016/j.cell.2012.01.058 · Cited by 2,043
A two-way street: reciprocal regulation of metabolism and signalling
Wellen, K. E., & Thompson, C. B. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3305 · Cited by 528
Chou, T.-Y., Hart, G. W., & Dang, C. V. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.32.18961 · Cited by 453
linking metabolism to epigenetics through O-GlcNAcylation
Hanover, J. A., Krause, M. W., & Love, D. C. (2012) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3334 · Cited by 414
Wellen, K. E., Lu, C., Mancuso, A., Lemons, J. M. S., Ryczko, M., Dennis, J. W., Rabinowitz, J. D., Coller, H. A., & Thompson, C. B. (2010) · Genes & Development · doi:10.1101/gad.1985910 · Cited by 377
Multiple pathways regulated by the tumor suppressor PP2A in transformation
Westermarck, J., & Hahn, W. C. (2008) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2008.02.001 · Cited by 344
Clinical significance of p53 alterations in surgically treated prostate cancers
Schlomm, T., Iwers, L., Kirstein, P., Jessen, B., Köllermann, J., Minner, S., Passow-Drolet, A., Mirlacher, M., Milde-Langosch, K., Graefen, M., et al. (2008) · Modern Pathology · doi:10.1038/modpathol.2008.104 · Cited by 196
Self-citationMoon, J.-S., Jin, W.-J., Kwak, J.-H., Kim, H.-J., Yun, M.-J., KIM, J.-W., Park, S. W., & Kim, K.-S. (2011) · Biochemical Journal · doi:10.1042/bj20101104 · Cited by 125
Cited by
The emerging hallmarks of cancer metabolism
Pavlova, N. N., & Thompson, C. B. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2015.12.006 · Cited by 5,926
Glycosylation in cancer: mechanisms and clinical implications
Pinho, S. S., & Reis, C. A. (2015) · Nature Reviews Cancer · doi:10.1038/nrc3982 · Cited by 3,083
Hallmarks of glycosylation in cancer
Munkley, J., & Elliott, D. J. (2016) · Oncotarget · doi:10.18632/oncotarget.8155 · Cited by 521
Fueling the fire: emerging role of the hexosamine biosynthetic pathway in cancer
Akella, N. M., Ciraku, L., & Reginato, M. J. (2019) · BMC Biology · doi:10.1186/s12915-019-0671-3 · Cited by 373
Protein Glycosylation and Tumor Microenvironment Alterations Driving Cancer Hallmarks
Peixoto, A., Relvas-Santos, M., Azevedo, R., Santos, L. L., & Ferreira, J. A. (2019) · Frontiers in Oncology · doi:10.3389/fonc.2019.00380 · Cited by 334
Metadata
- Authors
- Itkonen, H. M., Minner, S., Guldvik, I. J., Sandmann, M. J., Tsourlakis, M. C., Berge, V., Svindland, A., Schlomm, T., & Mills, I. G.
- Venue
- Cancer Research
- Published
- 2013-08-13
- Volume
- 73
- Issue
- 16
- Pages
- 5277-5287
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W2134468405
- Cited by
- 292
- References
- 10
- FWCI
- 8.07
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: O-GlcNAc Transferase Integrates Metabolic Pathways to Regulate the Stability of c-MYC in Human Prostate Cancer Cells. https://app.cochat.ai/papers/10.1158/0008-5472.can-13-0549
- The paper
- Itkonen, H. M., Minner, S., Guldvik, I. J., Sandmann, M. J., Tsourlakis, M. C., Berge, V., Svindland, A., Schlomm, T., & Mills, I. G. (2013). O-GlcNAc Transferase Integrates Metabolic Pathways to Regulate the Stability of c-MYC in Human Prostate Cancer Cells. Cancer Research. https://doi.org/10.1158/0008-5472.can-13-0549
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.