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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2005-12-23
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pubmed:abstractText |
The Polo-like kinases (Plks) are a highly conserved family of protein kinases that function in regulation of cell cycle and DNA damage-induced checkpoints. Evidence of a tumor suppressor function for the Plks in human neoplasia is lacking. Here, we report that Snk/Plk2 is transcriptionally down-regulated in B-cell neoplasms. Silencing occurs with very high frequency in Burkitt lymphoma (BL) but is also detected in B-cell neoplasms of other types and is associated with aberrant cytosine methylation in the CpG island located at the 5' end of the SNK/PLK2 gene. Silencing is specific to malignant B cells because SNK/PLK2 was unmethylated (and expressed) in primary B lymphocytes, in EBV-immortalized B lymphoblastoid cell lines (LCLs), and in adenocarcinomas (of the breast) and squamous-cell carcinomas (of the head and neck). Expression of Snk/Plk2 in BL cell lines was restored by demethylating agents. The related PLK1 and PLK3 (FNK/PRK) genes were overexpressed in BL cell lines lacking Snk/Plk2 expression, consistent with functional degeneracy among the Plk family. Ectopic expression of Snk/Plk2 in BL cells resulted in apoptosis, a potential mechanistic basis underlying the strong selective pressure for abrogation of Snk/Plk2 function in B-cell neoplasia.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0006-4971
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pubmed:author |
pubmed-author:AlldayMartinM,
pubmed-author:CrawfordDorothyD,
pubmed-author:CrookTimT,
pubmed-author:DyerMartinM,
pubmed-author:FarrellPaul JPJ,
pubmed-author:GriffinBeverleyB,
pubmed-author:HoffmannIngridI,
pubmed-author:KarranLorraineL,
pubmed-author:O'NionsJennyJ,
pubmed-author:SmithPaulP,
pubmed-author:SpenderLindsay CLC,
pubmed-author:SullivanAlexandraA,
pubmed-author:SyedNeloferN
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
107
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
250-6
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pubmed:dateRevised |
2011-11-2
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pubmed:meshHeading |
pubmed-meshheading:16160013-Apoptosis,
pubmed-meshheading:16160013-B-Lymphocytes,
pubmed-meshheading:16160013-Cell Cycle Proteins,
pubmed-meshheading:16160013-DNA Methylation,
pubmed-meshheading:16160013-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16160013-Gene Silencing,
pubmed-meshheading:16160013-Humans,
pubmed-meshheading:16160013-Leukemia, B-Cell,
pubmed-meshheading:16160013-Lymphoma, B-Cell,
pubmed-meshheading:16160013-Protein-Serine-Threonine Kinases,
pubmed-meshheading:16160013-Proto-Oncogene Proteins,
pubmed-meshheading:16160013-Transcription, Genetic,
pubmed-meshheading:16160013-Tumor Cells, Cultured
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pubmed:year |
2006
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pubmed:articleTitle |
Transcriptional silencing of Polo-like kinase 2 (SNK/PLK2) is a frequent event in B-cell malignancies.
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pubmed:affiliation |
Breakthrough Breast Cancer Centre, Institute of Cancer Research, Fulham Rd, London SW3 6JB, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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