Document Detail


Suppression of PI3K/mTOR pathway rescues LLC cells from cell death induced by hypoxia.
MedLine Citation:
PMID:  15781267     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cancer cells in solid tumors are challenged by various microenvironmental stresses, including hypoxia, and cancer cells in hypoxic regions are resistant to current cancer therapies. To investigate the mechanism of resistance to hypoxia in cancer cells, we examined mouse Lewis lung carcinoma (LLC) cells, which died due to necrosis at high density under hypoxic but not under normoxic conditions. Levels of mammalian target of rapamycin (mTOR), a central regulator of cellular energy, are reported to be suppressed in hypoxia. We found that phosphorylation of two molecules downstream to it, ribosomal p70 S6 kinase (S6K) and ribosomal protein S6, was markedly suppressed by hypoxia. Overexpression of the active form of S6K increased the sensitivity of LLC cells to hypoxia. On the other hand, inhibition of PI3K or mTOR dramatically reduced hypoxia-induced cell death under hypoxic conditions. Under hypoxic conditions, blockade of the PI3K or mTOR pathway increased levels of intracellular ATP and delayed decreases in pH and glucose level in culture medium, without affecting the cell cycle.
Authors:
Y Hamanaka; M Mukai; M Shimamura; T Kitagawa; T Nishida; F Isohashi; T Ito; Y Nishizawa; M Tatsuta; H Matsuda; M Inoue
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  330     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2005 Apr 
Date Detail:
Created Date:  2005-03-22     Completed Date:  2005-05-26     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  318-26     Citation Subset:  IM    
Affiliation:
Department of Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka, Japan.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / metabolism*
Adenosine Triphosphate / metabolism
Animals
Carcinoma, Lewis Lung / enzymology,  metabolism,  pathology*
Cell Death*
Cell Hypoxia*
Culture Media
Glucose / metabolism
Hydrogen-Ion Concentration
Mice
Necrosis
Phosphorylation
Protein Kinases / metabolism*
Ribosomal Protein S6 Kinases / metabolism
Tumor Cells, Cultured
Chemical
Reg. No./Substance:
0/Culture Media; 50-99-7/Glucose; 56-65-5/Adenosine Triphosphate; EC 2.7.-/Protein Kinases; EC 2.7.1.-/mTOR protein; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.11.1/Ribosomal Protein S6 Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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