Linked Life Data

15455373

Source:http://linkedlifedata.com/resource/pubmed/id/15455373

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-12-7
pubmed:abstractText
The gene product of spleen tyrosine kinase (SYK) has been implicated in the suppression of breast cancer invasion. We previously reported that SYK expression is lost in a subset of breast cancer; primarily by methylation-mediated gene silencing. In our study, we explored the possibility of using a DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (AZA), to suppress breast cancer cell invasion by restoring SYK expression. We found that AZA treatment reestablished the expression of SYK(L) that was accompanied by suppression of the invasion capacity of SYK-negative cells. This invasion inhibition was not due to global cellular toxicity since this treatment did not affect overall cell proliferation. This decreased invasiveness by AZA treatment was diminished by piceatannol, a SYK inhibitor, suggesting that SYK play a significant role in AZA-inducible invasion suppression. SYK promoter hypermethylation was found infrequent in pathologically normal mammary tissues or benign lesions (<5%). In contrast, SYK methylation was frequently identified in ductal carcinoma in situ ( approximately 45%) and invasive ductal carcinoma (47% in node-negative and 40% in node-positive cases), indicating that the hypermethylation of SYK occurs at a stage prior to the development of invasion phenotypes. All these results suggested a potential use of SYK methylation as a valuable biomarker to detect early cancerous lesions and support the use of AZA as a new reagent to the management of advanced breast cancer.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
113
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
654-9
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:15455373-Antimetabolites, Antineoplastic, pubmed-meshheading:15455373-Azacitidine, pubmed-meshheading:15455373-Breast, pubmed-meshheading:15455373-Breast Neoplasms, pubmed-meshheading:15455373-Carcinoma, Ductal, pubmed-meshheading:15455373-Carcinoma, Intraductal, Noninfiltrating, pubmed-meshheading:15455373-Cell Proliferation, pubmed-meshheading:15455373-DNA Methylation, pubmed-meshheading:15455373-DNA Modification Methylases, pubmed-meshheading:15455373-Enzyme Precursors, pubmed-meshheading:15455373-Female, pubmed-meshheading:15455373-Gene Expression Regulation, Neoplastic, pubmed-meshheading:15455373-Gene Silencing, pubmed-meshheading:15455373-Humans, pubmed-meshheading:15455373-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:15455373-Neoplasm Invasiveness, pubmed-meshheading:15455373-Phenotype, pubmed-meshheading:15455373-Protein-Tyrosine Kinases, pubmed-meshheading:15455373-Stilbenes
pubmed:year
2005
pubmed:articleTitle
Reactivation of SYK expression by inhibition of DNA methylation suppresses breast cancer cell invasiveness.
pubmed:affiliation
Department of Molecular Pathology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.