Document Detail


Synergism between altered cortical polarity and the PI3K/TOR pathway in the suppression of tumour growth.
MedLine Citation:
PMID:  22173033     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Loss of function of pins (partner of inscuteable) partially disrupts neuroblast (NB) polarity and asymmetric division, results in fewer and smaller NBs and inhibits Drosophila larval brain growth. Food deprivation also inhibits growth. However, we find that the combination of loss of function of pins and dietary restriction results in loss of NB asymmetry, overproliferation of Miranda-expressing cells, brain overgrowth and increased frequency of tumour growth on allograft transplantation. The same effects are observed in well-fed pins larvae that are mutant for pi3k (phosphatidylinositol 3-kinase) or exposed to the TOR inhibitor rapamycin. Thus, pathways that are sensitive to food deprivation and dependent on PI3K and TOR are essential to suppress tumour growth in Drosophila larval brains with compromised pins function. These results highlight an unexpected crosstalk whereby the normally growth-promoting, nutrient-sensing PI3K/TOR pathway suppresses tumour formation in neural stem cells with compromised cell polarity.
Authors:
Fabrizio Rossi; Cayetano Gonzalez
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-02-01
Journal Detail:
Title:  EMBO reports     Volume:  13     ISSN:  1469-3178     ISO Abbreviation:  EMBO Rep.     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-02-01     Completed Date:  2012-05-31     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  100963049     Medline TA:  EMBO Rep     Country:  England    
Other Details:
Languages:  eng     Pagination:  157-62     Citation Subset:  IM    
Affiliation:
Cell Division Group, Institute for Research in Biomedicine, Baldiri Reixac 10, 08028 Barcelona, Spain.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain Neoplasms / enzymology,  pathology*
Caloric Restriction
Cell Cycle Proteins / metabolism
Cell Polarity*
Cell Proliferation
Cerebral Cortex / enzymology*,  pathology*
Drosophila Proteins / antagonists & inhibitors,  metabolism*
Drosophila melanogaster / enzymology*
Energy Metabolism
Guanine Nucleotide Dissociation Inhibitors
Larva / growth & development,  metabolism
Mutation / genetics
Phosphatidylinositol 3-Kinase / metabolism*
Protein Kinases / metabolism*
Signal Transduction
Starvation
Stress, Physiological
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Drosophila Proteins; 0/Guanine Nucleotide Dissociation Inhibitors; 0/Mira protein, Drosophila; 0/Pins protein, Drosophila; EC 2.7.-/Protein Kinases; EC 2.7.1.-/target of rapamycin protein, Drosophila; EC 2.7.1.137/Phosphatidylinositol 3-Kinase
Comments/Corrections

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


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