Document Detail


Downregulation of Bim by brain-derived neurotrophic factor activation of TrkB protects neuroblastoma cells from paclitaxel but not etoposide or cisplatin-induced cell death.
MedLine Citation:
PMID:  16778834     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chemoresistance and increased expression of TrkB and brain-derived neurotrophic factor (BDNF) are biomarkers of poor prognosis in tumors from patients with neuroblastoma (NB). Previously, we found BDNF activation of TrkB through PI3K/Akt protects NB from etoposide/cisplatin-induced cell death. In this study, the role of Bim, a proapoptotic protein, was investigated. Bim was involved in paclitaxel but not etoposide or cisplatin-induced cell death in NB cells. Pharmacological and genetic studies showed that BDNF-induced decreases in Bim were regulated by MAPK and not PI3K/Akt pathway. Both MAPK and PI3K pathways were involved in BDNF protection of NB cells from paclitaxel-induced cell death, while PI3K predominantly mediated BDNF protection of NB cells from etoposide or cisplatin-induced cell death. These data indicate that different chemotherapeutic drugs induce distinct death pathways and growth factors utilize different signal transduction pathways to modulate the effects of chemotherapy on cells.
Authors:
Z Li; J Zhang; Z Liu; C-W Woo; C J Thiele
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural     Date:  2006-06-16
Journal Detail:
Title:  Cell death and differentiation     Volume:  14     ISSN:  1350-9047     ISO Abbreviation:  Cell Death Differ.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-01-15     Completed Date:  2007-03-16     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9437445     Medline TA:  Cell Death Differ     Country:  England    
Other Details:
Languages:  eng     Pagination:  318-26     Citation Subset:  IM    
Affiliation:
Cell & Molecular Biology Section, Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / metabolism
Antineoplastic Agents / pharmacology*
Apoptosis Regulatory Proteins / genetics,  metabolism*
Brain-Derived Neurotrophic Factor / pharmacology*
Cell Death / drug effects
Cisplatin / pharmacology
Down-Regulation / drug effects*
Enzyme Activation / drug effects
Etoposide / pharmacology
Forkhead Transcription Factors / metabolism
Gene Expression Regulation, Enzymologic / drug effects
Gene Expression Regulation, Neoplastic / drug effects
Gene Silencing
Humans
Membrane Proteins / genetics,  metabolism*
Mitogen-Activated Protein Kinases / metabolism
Molecular Mimicry / drug effects
Neuroblastoma / enzymology*,  genetics,  pathology*
Paclitaxel / pharmacology
Phosphorylation / drug effects
Protein Isoforms / genetics,  metabolism
Proto-Oncogene Proteins / genetics,  metabolism*
RNA, Messenger / genetics,  metabolism
RNA, Small Interfering / metabolism
Receptor, trkB / genetics,  metabolism*
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Apoptosis Regulatory Proteins; 0/Bcl-2-like protein 11; 0/Brain-Derived Neurotrophic Factor; 0/FOXO3 protein, human; 0/Forkhead Transcription Factors; 0/Membrane Proteins; 0/Protein Isoforms; 0/Proto-Oncogene Proteins; 0/RNA, Messenger; 0/RNA, Small Interfering; 15663-27-1/Cisplatin; 33069-62-4/Paclitaxel; 33419-42-0/Etoposide; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.10.1/Receptor, trkB; EC 2.7.11.24/Mitogen-Activated Protein Kinases

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


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