Document Detail


Src controls tumorigenesis via JNK-dependent regulation of the Hippo pathway in Drosophila.
MedLine Citation:
PMID:  23196366     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cell-cell interactions within the tumour microenvironment have crucial roles in epithelial tumorigenesis. Using Drosophila genetics, we show that the oncoprotein Src controls tumour microenvironment by Jun N-terminal kinase (JNK)-dependent regulation of the Hippo pathway. Clones of cells with elevated Src expression activate the Rac-Diaphanous and Ras-mitogen-activated protein kinase (MAPK) pathways, which cooperatively induce F-actin accumulation, thereby leading to activation of the Hippo pathway effector Yorkie (Yki). Simultaneously, Src activates the JNK pathway, which antagonizes the autonomous Yki activity and causes propagation of Yki activity to neighbouring cells, resulting in the overgrowth of surrounding tissue. Our data provide a mechanism to explain how oncogenic mutations regulate tumour microenvironment through cell-cell communication.
Authors:
Masato Enomoto; Tatsushi Igaki
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-11-30
Journal Detail:
Title:  EMBO reports     Volume:  14     ISSN:  1469-3178     ISO Abbreviation:  EMBO Rep.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-03     Completed Date:  2013-06-03     Revised Date:  2014-01-09    
Medline Journal Info:
Nlm Unique ID:  100963049     Medline TA:  EMBO Rep     Country:  England    
Other Details:
Languages:  eng     Pagination:  65-72     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Actins / genetics,  metabolism
Animals
Cell Communication
Cell Transformation, Neoplastic / genetics,  metabolism
Cells, Cultured
Drosophila Proteins / genetics,  metabolism*
Drosophila melanogaster / genetics,  metabolism*
Gene Expression Regulation
Humans
Intracellular Signaling Peptides and Proteins / genetics,  metabolism*
Larva / genetics,  metabolism*
MAP Kinase Kinase 4 / genetics,  metabolism*
Mitogen-Activated Protein Kinases / genetics,  metabolism
Models, Biological
Nuclear Proteins / genetics,  metabolism
Protein Binding
Protein-Serine-Threonine Kinases / genetics,  metabolism*
Signal Transduction*
Trans-Activators / genetics,  metabolism
Tumor Microenvironment
src-Family Kinases / genetics,  metabolism*
Chemical
Reg. No./Substance:
0/Actins; 0/Drosophila Proteins; 0/Intracellular Signaling Peptides and Proteins; 0/Nuclear Proteins; 0/Trans-Activators; 0/Yorkie protein, Drosophila; EC 2.7.10.2/src-Family Kinases; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/hpo protein, Drosophila; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 2.7.12.2/MAP Kinase Kinase 4
Comments/Corrections

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


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