Linked Life Data

15660112

Source:http://linkedlifedata.com/resource/pubmed/id/15660112

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2005-4-7
pubmed:abstractText
Basal cell carcinoma (BCC) is the most frequent cancer in the Caucasian population. Cells of BCC strongly express Fas-ligand (FasL), a member of the tumor necrosis family, which induces apoptosis in Fas receptor-expressing cells. It has been suggested that by expression of FasL, BCC cells may evade the attack of Fas-positive immune effector cells allowing the tumor to expand. Thus, downregulation of FasL should prime BCC to the assault of immune effector cells. Recently, it has been shown that RNA interference is a highly successful approach to specifically silence a gene of interest in single cells and some animal models. However, RNAi in human tissues has not been shown so far. Here, we provide evidence that small interfering RNAs (siRNAs) efficiently transfect tumor tissue ex vivo and silence the gene of interest. We demonstrate that a specific siRNA efficiently downregulates FasL not only in FasL-positive indicator cells but also in surgically excised BCC tissue at both the protein and the mRNA level. The successful transfection of tumor tissues with siRNAs now allows to test the function of the molecule under study and opens up the investigation of other target genes in the tumor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0969-7128
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
678-84
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Fas-ligand gene silencing in basal cell carcinoma tissue with small interfering RNA.
pubmed:affiliation
Institute for Medical Microbiology, University of Basel, Basel, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't