Document Detail


Elimination of oncogenic neighbors by JNK-mediated engulfment in Drosophila.
MedLine Citation:
PMID:  21397843     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A newly emerged oncogenic cell in the epithelial population has to confront antitumor selective pressures in the host tissue. However, the mechanisms by which surrounding normal tissue exerts antitumor effects against oncogenically transformed cells are poorly understood. In Drosophila imaginal epithelia, clones of cells mutant for evolutionarily conserved tumor suppressor genes such as scrib or dlg lose their epithelial integrity and are eliminated from epithelia when surrounded by wild-type tissue. Here, we show that surrounding normal cells activate nonapoptotic JNK signaling in response to the emergence of oncogenic mutant cells. This JNK activation leads to upregulation of PVR, the Drosophila PDGF/VEGF receptor. Genetic and time-lapse imaging analyses reveal that PVR expression in surrounding cells activates the ELMO/Mbc-mediated phagocytic pathway, thereby eliminating oncogenic neighbors by engulfment. Our data indicate that JNK-mediated cell engulfment could be an evolutionarily conserved intrinsic tumor-suppression mechanism that eliminates premalignant cells from epithelia.
Authors:
Shizue Ohsawa; Kaoru Sugimura; Kyoko Takino; Tian Xu; Atsushi Miyawaki; Tatsushi Igaki
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Developmental cell     Volume:  20     ISSN:  1878-1551     ISO Abbreviation:  Dev. Cell     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-03-14     Completed Date:  2011-05-12     Revised Date:  2012-06-04    
Medline Journal Info:
Nlm Unique ID:  101120028     Medline TA:  Dev Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  315-28     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Affiliation:
Department of Cell Biology, G-COE, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Signal Transducing / genetics,  metabolism
Animals
Drosophila Proteins / genetics,  metabolism*
Drosophila melanogaster / anatomy & histology*,  embryology*,  metabolism
Enzyme Activation
Epithelium / embryology,  metabolism
JNK Mitogen-Activated Protein Kinases / genetics,  metabolism*
Membrane Proteins / genetics,  metabolism
Neoplasms / pathology,  physiopathology
Oncogenes*
Phagocytosis / physiology*
Receptor Protein-Tyrosine Kinases / genetics,  metabolism
Recombinant Fusion Proteins / genetics,  metabolism
Signal Transduction / physiology
Tumor Suppressor Proteins / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Drosophila Proteins; 0/ELMO protein, Drosophila; 0/Membrane Proteins; 0/Recombinant Fusion Proteins; 0/Tumor Suppressor Proteins; 0/eiger protein, Drosophila; 0/scribbled protein, Drosophila; EC 2.7.10.1/Pvr protein, Drosophila; EC 2.7.10.1/Receptor Protein-Tyrosine Kinases; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases
Comments/Corrections
Comment In:
Nat Rev Cancer. 2011 May;11(5):314   [PMID:  21508967 ]

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