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O-GlcNAc protein modification in cancer cells increases in response to glucose deprivation through glycogen degradation

Authors
 Jeong Gu Kang  ;  Sang Yoon Park  ;  Suena Ji  ;  Insook Jang  ;  Sujin Park  ;  Hyun Sil Kim  ;  Sung-Min Kim  ;  Jong In Yook  ;  Yong-Il Park  ;  Ju¨rgen Roth  ;  Jin Won Cho 
Citation
 JOURNAL OF BIOLOGICAL CHEMISTRY, Vol.284(50) : 34777-34784, 2009 
Journal Title
 JOURNAL OF BIOLOGICAL CHEMISTRY 
ISSN
 0021-9258 
Issue Date
2009
MeSH
AMP-Activated Protein Kinases/metabolism ; Acetylglucosamine/metabolism* ; Animals ; Cell Line ; Glucose/metabolism* ; Glycogen/metabolism* ; Humans ; N-Acetylglucosaminyltransferases/metabolism ; Neoplasms/metabolism* ; Protein Processing, Post-Translational*
Abstract
When cellular glucose concentrations fall below normal levels, in general the extent of protein O-GlcNAc modification (O-GlcNAcylation) decreases. However, recent reports demonstrated increased O-GlcNAcylation by glucose deprivation in HepG2 and Neuro-2a cells. Here, we report increased O-GlcNAcylation in non-small cell lung carcinoma A549 cells and various other cells in response to glucose deprivation. Although the level of O-GlcNAc transferase was unchanged, the enzyme contained less O-GlcNAc, and its activity was increased. Moreover, O-GlcNAcase activity was reduced. The studied cells contain glycogen, and we show that its degradation in response to glucose deprivation provides a source for UDP-GlcNAc required for increased O-GlcNAcylation under this condition. This required active glycogen phosphorylase and resulted in increased glutamine:fructose-6-phosphate amidotransferase, the first and rate-limiting enzyme in the hexosamine biosynthetic pathway. Interestingly, glucose deprivation reduced the amount of phosphofructokinase 1, a regulatory glycolytic enzyme, and blocked ATP synthesis. These findings suggest that glycogen is the source for increased O-GlcNAcylation but not for generating ATP in response to glucose deprivation and that this may be useful for cancer cells to survive.
Files in This Item:
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DOI
10.1074/jbc.M109.026351
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Pathology (구강병리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Hyun Sil(김현실) ORCID logo https://orcid.org/0000-0003-3614-1764
Yook, Jong In(육종인) ORCID logo https://orcid.org/0000-0002-7318-6112
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/105665
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