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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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OGA heterozygosity suppresses intestinal tumorigenesis in Apc min/+ mice

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Title
OGA heterozygosity suppresses intestinal tumorigenesis in Apc min/+ mice
Author
Yang, YongryoulJang H.J.Yoon, SunyoungLee, YonghwaNam, DouguKim, I.S.Lee, HeeseokKim, HyunChoi, Jang HyunKang, Byoung HeonRyu, SunghoSuh, Pann-Ghill
Keywords
O-GLCNAC TRANSFERASE; BETA-N-ACETYLGLUCOSAMINE; PROSTATE-CANCER CELLS; GLCNACYLATION; METASTASIS; STABILITY; CATENIN; PHOSPHORYLATION; TRANSCRIPTION; LOCALIZATION
Issue Date
201407
Publisher
Nature Publishing Group
Citation
Oncogenesis, v.3, no., pp.1 - 6
Abstract
Emerging evidence suggests that aberrant O-GlcNAcylation is associated with tumorigenesis. Many oncogenic factors are O-GlcNAcylated, which modulates their functions. However, it remains unclear how O-GlcNAcylation and O-GlcNAc cycling enzymes, O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), affect the development of cancer in animal models. In this study, we show that reduced level of OGA attenuates colorectal tumorigenesis induced by Adenomatous polyposis coli (Apc) mutation. The levels of O-GlcNAcylation and O-GlcNAc cycling enzymes were simultaneously upregulated in intestinal adenomas from mice, and in human patients. In two independent microarray data sets, the expression of OGA and OGT was significantly associated with poor cancer-specific survival of colorectal cancer (CRC) patients. In addition, OGA heterozygosity, which results in increased levels of O-GlcNAcylation, attenuated intestinal tumor formation in the Apc min/+ background. Apc min/+ OGA +/-mice exhibited a significantly increased survival rate compared with Apc min/+ mice. Consistent with this, Apc min/+ OGA +/-mice expressed lower levels of Wnt target genes than Apc min/+. However, the knockout of OGA did not affect Wnt/β-catenin signaling. Overall, these findings suggest that OGA is crucial for tumor growth in CRC independently of Wnt/β-catenin signaling.
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DOI
http://dx.doi.org/10.1038/oncsis.2014.24
ISSN
2157-9024
Appears in Collections:
SLS_Journal Papers
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