Source:http://linkedlifedata.com/resource/pubmed/id/19652203
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
13
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pubmed:dateCreated |
2009-9-25
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pubmed:abstractText |
Multiple myeloma (MM) is a cancer of plasma cells with complex molecular characteristics that evolves from monoclonal gammopathy of undetermined significance, a highly prevalent premalignant condition. MM is the second most frequent hematologic cancer in the United States, and it remains incurable, thereby highlighting the need for new therapeutic approaches, particularly those targeting common molecular pathways involved in disease progression and maintenance, shared across different MM subtypes. Here we report that Wnt/beta-catenin is one such pathway. We document the involvement of beta-catenin in cell-cycle regulation, proliferation, and invasion contributing to enhanced proliferative and metastatic properties of MM. The pleiotropic effects of beta-catenin in MM correlate with its transcriptional function, and we demonstrate regulation of a novel target gene, Aurora kinase A, implicating beta-catenin in G2/M regulation. beta-catenin and Aurora kinase A are present in most MM but not in normal plasma cells and are expressed in a pattern that parallels progression from monoclonal gammopathy of undetermined significance to MM. Our data provide evidence for a novel functional link between beta-catenin and Aurora kinase A, underscoring a critical role of these pathways in MM disease progression.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1528-0020
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pubmed:author |
pubmed-author:AndersonKenneth CKC,
pubmed-author:CarlsonNicole ENE,
pubmed-author:CarrascoDaniel EDE,
pubmed-author:CarrascoDaniel RDR,
pubmed-author:Dutta-SimmonsJuiJ,
pubmed-author:GattMosheM,
pubmed-author:GorgunGulluG,
pubmed-author:HideshimaTeruT,
pubmed-author:LEEO SOSJr,
pubmed-author:LetaiAnthony GAG,
pubmed-author:RajeNoopurN,
pubmed-author:TaiYu-TzuYT,
pubmed-author:TakadaKohichiK,
pubmed-author:ZhangYunyuY
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pubmed:issnType |
Electronic
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pubmed:day |
24
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pubmed:volume |
114
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2699-708
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pubmed:dateRevised |
2011-7-11
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pubmed:meshHeading |
pubmed-meshheading:19652203-Animals,
pubmed-meshheading:19652203-Cell Cycle,
pubmed-meshheading:19652203-Cell Proliferation,
pubmed-meshheading:19652203-Disease Progression,
pubmed-meshheading:19652203-Drug Resistance, Neoplasm,
pubmed-meshheading:19652203-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:19652203-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:19652203-Humans,
pubmed-meshheading:19652203-Mice,
pubmed-meshheading:19652203-Mice, Inbred NOD,
pubmed-meshheading:19652203-Mice, SCID,
pubmed-meshheading:19652203-Mice, Transgenic,
pubmed-meshheading:19652203-Multiple Myeloma,
pubmed-meshheading:19652203-Protein-Serine-Threonine Kinases,
pubmed-meshheading:19652203-Transplantation, Heterologous,
pubmed-meshheading:19652203-Tumor Cells, Cultured,
pubmed-meshheading:19652203-Wnt Proteins,
pubmed-meshheading:19652203-beta Catenin
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pubmed:year |
2009
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pubmed:articleTitle |
Aurora kinase A is a target of Wnt/beta-catenin involved in multiple myeloma disease progression.
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pubmed:affiliation |
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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