Document Detail


3-phosphoinositide-dependent protein kinase-1 regulates proliferation and survival of cancer cells with an activated mitogen-activated protein kinase pathway.
MedLine Citation:
PMID:  20197379     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Engagement of cell surface receptor tyrosine kinases by insulin and growth factors activates phosphatidylinositol 3-kinase (PI3K) and generates the second messenger, phosphatidylinositol 3,4,5-trisphosphate. This second messenger leads to the recruitment of 3-phosphoinositide-dependent protein kinase-1 (PDK1) to the proximal side of the plasma membrane, which results in the activation of AKT kinase. In addition, PDK1 can phosphorylate numerous other kinases, including p90RSK, a kinase downstream of mitogen-activated protein kinase (MAPK) that is important for cell proliferation and survival. Previous studies have shown that the loss of PDK1 sensitizes tumor cells to chemotherapeutic agents and radiation but have not focused on delineating the contribution of PDK1 to pathway-specific mutations associated with various cancers other than the PI3K/AKT pathway. In this study, we show that the reduction of PDK1 by RNAi in melanoma and colon cancer cell lines activated in the MAPK pathway results in significant cell growth inhibition and apoptosis. Furthermore, PDK1 reduction in tumor cells resulted in impaired PAK kinase signaling, altered actin polymerization, and reduced cell migration. These studies show that PDK1 plays a pivotal role in MAPK and PI3K signaling in tumor cells.
Authors:
Zhuomei Lu; Mary Ann Cox-Hipkin; William T Windsor; Anita Boyapati
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Publication Detail:
Type:  Journal Article     Date:  2010-03-02
Journal Detail:
Title:  Molecular cancer research : MCR     Volume:  8     ISSN:  1557-3125     ISO Abbreviation:  Mol. Cancer Res.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-18     Completed Date:  2010-07-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101150042     Medline TA:  Mol Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  421-32     Citation Subset:  IM    
Affiliation:
Schering-Plough Research Institute, Kenilworth, NJ 07033, USA.
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MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / genetics,  metabolism*
Apoptosis / genetics
Carcinoma / enzymology,  genetics
Cell Line, Tumor
Cell Proliferation*
Cell Survival / genetics
Colonic Neoplasms / enzymology,  genetics
Down-Regulation / genetics
Enzyme Activation / genetics
Gene Expression Regulation, Enzymologic / genetics
Gene Expression Regulation, Neoplastic / genetics
Humans
MAP Kinase Signaling System / genetics
Melanoma / enzymology,  genetics
Neoplasms / enzymology*,  genetics
Phosphatidylinositol Phosphates / metabolism
Protein-Serine-Threonine Kinases / genetics,  metabolism*
RNA Interference / physiology
Chemical
Reg. No./Substance:
0/Phosphatidylinositol Phosphates; 0/phosphatidylinositol 3,4,5-triphosphate; EC 2.7.1.-/3-phosphoinositide-dependent protein kinase; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.11.1/Protein-Serine-Threonine Kinases

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


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