Document Detail

PTEN/pAkt/p53 signaling pathway correlates with the radioresponse of non-small cell lung cancer.
MedLine Citation:
PMID:  20198299     Owner:  NLM     Status:  MEDLINE    
The sensitivity or resistance of cancer cells and normal tissues to ionizing radiation plays an important role in the clinical setting of lung cancer treatment. However, to date the exact molecular mechanisms of intrinsic radiosensitivity have not been well explained. In this study, we compared the radiosensitivity or radioresistance in two non-small cell lung cancers (NSCLCs), H460 and A549, and investigated the signaling pathways that confer radioresistance. H460 cells showed a significant G(2)/M arrest after 12 h of irradiation (5 Gy), reaching 60% of G(2)/M phase arrest. A549 cells also showed a significant G(2)/M arrest after 12 h of exposure; however, this arrest completely disappeared after 24 h of exposure. A549 has higher methylated CpG sites in PTEN, which is correlated with tumor radioresistance in some cancer cells, than H460 cells, and the average of the extent of the methylation was approximately 4.3 times higher in A549 cells than in H460 cells. As a result, PTEN expression was lower in A549 than in H460. Conducting Western blot analysis, we found that PTEN acted as a negative regulator for pAkt, and the pAkt acted as a negative regulator for p53 expression. According to the above results, we concluded that the radiosensitivity shown in H460 cells may be due to the higher expression of PTEN through p53 signaling pathway.
Il Lae Jung; Hyo Jin Kang; Kug Chan Kim; In Gyu Kim
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of molecular medicine     Volume:  25     ISSN:  1791-244X     ISO Abbreviation:  Int. J. Mol. Med.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-03-03     Completed Date:  2010-05-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9810955     Medline TA:  Int J Mol Med     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  517-23     Citation Subset:  IM    
Department of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute, Yuseong, Daejeon 305-600, Korea.
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MeSH Terms
Base Sequence
Blotting, Western
Carcinoma, Non-Small-Cell Lung / enzymology*,  pathology,  radiotherapy
Cell Death / radiation effects
Cell Line, Tumor
CpG Islands / genetics
DNA Methylation / genetics,  radiation effects
G2 Phase / radiation effects
Lung Neoplasms / enzymology*,  pathology,  radiotherapy
Mitosis / radiation effects
PTEN Phosphohydrolase / genetics,  metabolism*
Proto-Oncogene Proteins c-akt / metabolism*
Radiation Tolerance* / radiation effects
Radiation, Ionizing
Sequence Analysis, DNA
Signal Transduction* / radiation effects
Tumor Suppressor Protein p53 / metabolism*
Reg. No./Substance:
0/Tumor Suppressor Protein p53; EC Proteins c-akt; EC protein, human; EC Phosphohydrolase

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