| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Papers In Press, published online ahead of print June 28, 2002
Investigative Treatment Division, National Cacer Center Research Institute East, Kashiwa, Chiba
Corresponding Author: hesumi{at}east.ncc.go.jp
Hypoxia is a critical event for higher organisms, and cells and tissues react by increasing the oxygen supply by vasodilatation, angiogenesis, and erythropoiesis and maintaining cellular energy by increasing glycolysis and inhibiting anabolic pathways. Stimulation of glycolysis has been regarded as the main response that increases energy production during hypoxia, however, there is an obvious conflict during ischemia, because both the oxygen and glucose supply are insufficient. In this study, we found that exposure of HepG2 cells and normal fibroblasts to hypoxia induces cellular tolerance to glucose starvation. The tolerance induced by hypoxia is dependent on several amino acids, indicating switch from glucose to amino acids as the energy source. When antisense RNA expression vector for 5’-AMP-activated protein kinase or PKB/Akt was transfected into HepG2 cells, the induction of tolerance to glucose was greatly inhibited, indicating that the tolerance was dependent on 5’-AMP activated protein kinase and PKB/Akt. Similar tolerance was induced by nitric oxide exposure. The tolerance induced was observed in various cells and may represent a previously unknown physiological response related to hypoxia-preconditioning and tumor progression:austerity.
J. Biol. Chem, 10.1074/jbc.M112270200
Submitted on December 21, 2001
Revised on June 26, 2002
Accepted on June 27, 2002
Hypoxia and nitric oxide treatment confer tolerance to glucose starvation in a 5?f-AMP-activated protein kinase-dependent manner
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  H.-S. Kim, J.-T. Hwang, H. Yun, S.-G. Chi, S.-J. Lee, I. Kang, K.-S. Yoon, W.-J. Choe, S.-S. Kim, and J. Ha Inhibition of AMP-activated Protein Kinase Sensitizes Cancer Cells to Cisplatin-induced Apoptosis via Hyper-induction of p53 J. Biol. Chem., February 15, 2008; 283(7): 3731 - 3742. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Sato, K. Tsuchihara, S. Fujii, M. Sugiyama, T. Goya, Y. Atomi, T. Ueno, A. Ochiai, and H. Esumi Autophagy Is Activated in Colorectal Cancer Cells and Contributes to the Tolerance to Nutrient Deprivation Cancer Res., October 15, 2007; 67(20): 9677 - 9684. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.-C. Hsu, H.-C. Lee, Y.-H. Ping, T.-Y. Liu, W.-Y. Lui, and C.-W. Chi Mitochondria Are an Essential Mediator of Nitric Oxide/Cyclic Guanosine 3',5'-Monophosphate Blocking of Glucose Depletion Induced Cytotoxicity in Human HepG2 Cells Mol. Cancer Res., September 1, 2007; 5(9): 923 - 932. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. B. Nicoud, C. D. Knox, C. M. Jones, C. D. Anderson, J. M. Pierce, A. E. Belous, T. M. Earl, and R. S. Chari 2-APB protects against liver ischemia-reperfusion injury by reducing cellular and mitochondrial calcium uptake Am J Physiol Gastrointest Liver Physiol, September 1, 2007; 293(3): G623 - G630. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Cui, S. Darmanin, M. Natsuisaka, T. Kondo, M. Asaka, M. Shindoh, F. Higashino, J. Hamuro, F. Okada, M. Kobayashi, et al. Enhanced Expression of Asparagine Synthetase under Glucose-Deprived Conditions Protects Pancreatic Cancer Cells from Apoptosis Induced by Glucose Deprivation and Cisplatin Cancer Res., April 1, 2007; 67(7): 3345 - 3355. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. R. Laderoute, K. Amin, J. M. Calaoagan, M. Knapp, T. Le, J. Orduna, M. Foretz, and B. Viollet 5'-AMP-Activated Protein Kinase (AMPK) Is Induced by Low-Oxygen and Glucose Deprivation Conditions Found in Solid-Tumor Microenvironments. Mol. Cell. Biol., July 1, 2006; 26(14): 5336 - 5347. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Suzuki, T. Ogura, and H. Esumi NDR2 Acts as the Upstream Kinase of ARK5 during Insulin-like Growth Factor-1 Signaling J. Biol. Chem., May 19, 2006; 281(20): 13915 - 13921. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. C. Land and C. Rae iNOS initiates and sustains metabolic arrest in hypoxic lung adenocarcinoma cells: mechanism of cell survival in solid tumor core Am J Physiol Cell Physiol, October 1, 2005; 289(4): C918 - C933. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Suzuki, G.-i. Kusakai, Y. Shimojo, J. Chen, T. Ogura, M. Kobayashi, and H. Esumi Involvement of Transforming Growth Factor-{beta}1 Signaling in Hypoxia-induced Tolerance to Glucose Starvation J. Biol. Chem., September 9, 2005; 280(36): 31557 - 31563. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Suzuki, J. Lu, G.-i. Kusakai, A. Kishimoto, T. Ogura, and H. Esumi ARK5 Is a Tumor Invasion-Associated Factor Downstream of Akt Signaling Mol. Cell. Biol., April 15, 2004; 24(8): 3526 - 3535. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. G. Rajendran, D. A. Mankoff, F. O'Sullivan, L. M. Peterson, D. L. Schwartz, E. U. Conrad, A. M. Spence, M. Muzi, D. G. Farwell, and K. A. Krohn Hypoxia and Glucose Metabolism in Malignant Tumors: Evaluation by [18F]Fluoromisonidazole and [18F]Fluorodeoxyglucose Positron Emission Tomography Imaging Clin. Cancer Res., April 1, 2004; 10(7): 2245 - 2252. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G.-i. Kusakai, A. Suzuki, T. Ogura, S.'i. Miyamoto, A. Ochiai, M. Kaminishi, and H. Esumi ARK5 Expression in Colorectal Cancer and Its Implications for Tumor Progression Am. J. Pathol., March 1, 2004; 164(3): 987 - 995. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Suzuki, G.-i. Kusakai, A. Kishimoto, J. Lu, T. Ogura, M. F. Lavin, and H. Esumi Identification of a Novel Protein Kinase Mediating Akt Survival Signaling to the ATM Protein J. Biol. Chem., January 3, 2003; 278(1): 48 - 53. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
