Document Detail


Apoptosis resistance and PKC signaling: distinguishing features of high and low metastatic cells.
MedLine Citation:
PMID:  22496624     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The complexity of the process of metastasis is widely recognized. We report herein on a recurrent feature of high compared to low metastatic cells that is linked to their ability to survive early after their arrival at secondary sites. Using novel fluorescent-based imaging strategies that assess tumor cell interaction with the lung microenvironment, we have determined that most high and low metastatic cells can be distinguished within 6 hours of their arrival in the lung and further that this difference is defined by the ability of high metastatic cells to resist apoptosis at the secondary site. Despite the complexity of the metastatic cascade, the performance of cells during this critical window is highly defining of their metastatic proclivity. To explore mechanisms, we next evaluated biochemical pathways that may be linked to this survival phenotype in highly metastatic cells. Interestingly, we found no association between the Akt survival pathway and this metastatic phenotype. Of all pathways examined, only protein kinase C (PKC) activation was significantly linked to survival of highly metastatic cells. These data provide a conceptual understanding of a defining difference between high and low metastatic cells. The connection to PKC activation may provide a biologic rationale for the use of PKC inhibition in the prevention of metastatic progression.
Authors:
Sung-Hyeok Hong; Ling Ren; Arnulfo Mendoza; Ananth Eleswarapu; Chand Khanna
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural    
Journal Detail:
Title:  Neoplasia (New York, N.Y.)     Volume:  14     ISSN:  1476-5586     ISO Abbreviation:  Neoplasia     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-04-12     Completed Date:  2012-08-07     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  100886622     Medline TA:  Neoplasia     Country:  Canada    
Other Details:
Languages:  eng     Pagination:  249-58     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Neoplasia Press, Inc.
Affiliation:
Tumor and Metastasis 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:
Animals
Apoptosis* / genetics
Cell Line, Tumor
Cell Proliferation / drug effects
Female
Humans
Lung Neoplasms / drug therapy,  metabolism,  secondary*
Mice
Mice, Inbred BALB C
Neoplasms / genetics,  metabolism*,  pathology
Phenotype
Protein Kinase C / antagonists & inhibitors,  metabolism*
Protein Kinase Inhibitors / administration & dosage,  pharmacology
Proto-Oncogene Proteins c-akt / genetics,  metabolism
Signal Transduction* / drug effects
Chemical
Reg. No./Substance:
0/Protein Kinase Inhibitors; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.13/Protein Kinase C
Comments/Corrections

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