Document Detail


Reactive oxygen species and lipoxygenases regulate the oncogenicity of NPM-ALK-positive anaplastic large cell lymphomas.
MedLine Citation:
PMID:  19503098     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The chimera nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), the tyrosine kinase activity of which is constitutively upregulated, is the causative agent of 75% of the anaplastic large-cell lymphomas (ALCLs). We have demonstrated that NPM-ALK induces the production of reactive oxygen species (ROS) by a pathway involving the arachidonic acid-metabolizing enzymes of the lipoxygenase (LOX) family. The use of the LOX inhibitor nordihydroguaiaretic acid (NDGA) and of the anti-oxidant N-acetylcysteine (NAC) demonstrated that ROS are important in maintaining the ALK kinase active. Consistent with this, NDGA treatment resulted in the inhibition of key pathways, such as Akt, signal transducer and activator of transcription factor 3 (STAT3) and extracellular signal-regulated kinase (ERK), which are involved in NPM-ALK antiapoptotic and pro-mitogenic functions. Conversely, the stress-activated kinase p38, described in some instances as a mediator of apoptosis, was activated. Interestingly, 5-LOX, an isoform involved in many cancers, was found to be activated in NPM-ALK(+) cells. Functional studies have shown that transforming properties, namely proliferation and resistance to apoptosis, were abrogated by treatment with either NDGA or the 5-LOX inhibitor (N-(3-phenoxycinnamyl)-acetohydroxamic acid) (BW A4C). Together, these data point to the ROS/LOX pathway as a potential new target for therapy in NPM-ALK-positive tumors.
Authors:
K Thornber; A Colomba; L Ceccato; G Delsol; B Payrastre; F Gaits-Iacovoni
Related Documents :
21059648 - Pigment epithelium-derived factor and its phosphomimetic mutant induce jnk-dependent ap...
22403078 - Phosphoinositide phosphatases: just as important as the kinases.
7501988 - Cross-linking of cell surface receptors as a trigger or cell apoptosis and proliferation.
11520058 - Arsenic trioxide induces g2/m growth arrest and apoptosis after caspase-3 activation an...
21807898 - Antagonistic regulation of cystic fibrosis transmembrane conductance regulator cell sur...
8759518 - Differential phosphorylation of alpha-a crystallin in human lens of different age.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-06-08
Journal Detail:
Title:  Oncogene     Volume:  28     ISSN:  1476-5594     ISO Abbreviation:  Oncogene     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-07-23     Completed Date:  2009-08-10     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  2690-6     Citation Subset:  IM    
Affiliation:
INSERM, U563, Département Oncogénèse, Signalisation et Innovation Thérapeutique, Toulouse, France.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Apoptosis
Arachidonate 5-Lipoxygenase / antagonists & inhibitors,  metabolism*
Cell Line, Tumor
Humans
Lipoxygenase Inhibitors / pharmacology
Lymphoma, Large-Cell, Anaplastic / enzymology,  pathology*
Nordihydroguaiaretic Acid / analysis
Protein-Tyrosine Kinases / metabolism*
Reactive Oxygen Species / metabolism*
Chemical
Reg. No./Substance:
0/Lipoxygenase Inhibitors; 0/Reactive Oxygen Species; 500-38-9/Nordihydroguaiaretic Acid; EC 1.13.11.34/Arachidonate 5-Lipoxygenase; EC 2.7.1.-/p80(NPM-ALK) protein; EC 2.7.10.1/Protein-Tyrosine Kinases

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


Previous Document:  Defective expression of polarity protein PAR-3 gene (PARD3) in esophageal squamous cell carcinoma.
Next Document:  Methylation profiles of 22 candidate genes in breast cancer using high-throughput MALDI-TOF mass arr...