Document Detail


Resistance to chemotherapeutic agents and promotion of transforming activity mediated by embryonic stem cell-expressed Ras (ERas) signal in neuroblastoma cells.
MedLine Citation:
PMID:  20811723     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Neuroblastoma is a common childhood tumor derived from neural crest precursor cells. In the present study, we investigated the expression and function of embryonic stem cell-expressed Ras (ERas), a novel Ras family protein previously reported as the specific expression gene in embryonic stem cells (ES cells), in neuroblastoma cell lines. Our results showed that the expressions of ERas were detected in neuroblastoma cell lines by RT-PCR and Western blotting. Therefore, we transfected a full length ERas expression vector into the neuroblastoma cell line SH-SY5Y, which has weak endogenous expression of ERas, and obtained clones with higher levels of expression. Overexpression of ERas did not increase the growth rate of the ERas transfectants but promoted their transforming activity. The ERas transfectants were more resistant to all the chemotherapy agents than the parental cell line. The ability of ERas to rescue cells from the toxic effect of chemotherapeutic agents was inhibited by the phosphatidylinositol 3'-kinase (PI3K) inhibitor PD294002. These results show that the ERas/PI3K pathway may provide resistance to chemotherapy and promote transforming activity in neuroblastoma.
Authors:
Mineyoshi Aoyama; Hiromi Kataoka; Eiji Kubota; Toyohiro Tada; Kiyofumi Asai
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of oncology     Volume:  37     ISSN:  1791-2423     ISO Abbreviation:  Int. J. Oncol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-02     Completed Date:  2010-12-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9306042     Medline TA:  Int J Oncol     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  1011-6     Citation Subset:  IM    
Affiliation:
Department of Molecular Neurobiology, Nagoya City University Graduate School of Medical Sciences, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan. ao.mine@med.nagoya-cu.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Antineoplastic Agents / pharmacology*
Blotting, Western
Cell Line, Tumor
Cell Proliferation / drug effects
Cell Survival / drug effects
Cell Transformation, Neoplastic / genetics,  metabolism*
Cisplatin / pharmacology
Doxorubicin / pharmacology
Drug Resistance, Neoplasm* / genetics
Etoposide / pharmacology
Humans
Neuroblastoma / genetics,  metabolism*,  pathology
Oncogene Protein p21(ras) / genetics,  metabolism*
Phosphatidylinositol 3-Kinases / antagonists & inhibitors,  metabolism
Protein Kinase Inhibitors / pharmacology
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction / drug effects*
Time Factors
Transfection
Vinblastine / pharmacology
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/ERas protein, human; 0/Protein Kinase Inhibitors; 15663-27-1/Cisplatin; 23214-92-8/Doxorubicin; 33419-42-0/Etoposide; 865-21-4/Vinblastine; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 3.6.5.2/Oncogene Protein p21(ras)

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