| pubmed-article:17514651 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17514651 | lifeskim:mentions | umls-concept:C0079427 | lld:lifeskim |
| pubmed-article:17514651 | lifeskim:mentions | umls-concept:C0017636 | lld:lifeskim |
| pubmed-article:17514651 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
| pubmed-article:17514651 | lifeskim:mentions | umls-concept:C0524869 | lld:lifeskim |
| pubmed-article:17514651 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:17514651 | lifeskim:mentions | umls-concept:C0002345 | lld:lifeskim |
| pubmed-article:17514651 | lifeskim:mentions | umls-concept:C1537486 | lld:lifeskim |
| pubmed-article:17514651 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:17514651 | pubmed:dateCreated | 2007-7-30 | lld:pubmed |
| pubmed-article:17514651 | pubmed:abstractText | Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor and possesses a high incidence of 10p loss. The KLF6 (Kruppel-like transcription factor) tumor suppressor gene on 10p15 is inactivated by loss of heterozygosity (LOH) and/or somatic mutation in a number of human cancers and forced expression of KLF6 in GBM lines inhibits their growth and transformation. In addition, increased expression of its alternatively spliced, cytoplasmic isoform KLF6-SV1 has now been shown to play a role in cancer pathogenesis. On the basis of these findings we examined the role of KLF6 and KLF6-SV1 in the development and progression of GBM. LOH analysis of 17 primary GBM patient samples using KLF6-specific microsatellite markers revealed that 88.2% (15/17) had LOH of the KLF6 locus. Interestingly, no KLF6 somatic mutations were identified. RNA analysis revealed concomitant decreases in all primary GBM tumors (n = 11) by approximately 80% in KLF6 expression (p < 0.001) coupled with increased KLF6-SV1 expression (p < 0.001) when compared to normal astrocytes. To determine the biological relevance of these findings, we examined the effect of KLF6 expression and KLF6-SV1 knockdown in A235 and CRL2020 cell lines. Reconstitution of KLF6 decreased cell proliferation by almost 50%, whereas targeted KLF6 reduction increased cell proliferation 2.5-4.5 fold. Conversely, targeted KLF6-SV1 reduction decreased cell proliferation by 50%. Taken together, our findings demonstrate that KLF6 allelic imbalance and decreased KLF6 and increased KLF6-SV1 expression are common findings in primary GBM tumors, and these changes have antagonistic effects on the regulation of cellular proliferation in GBM cell lines. | lld:pubmed |
| pubmed-article:17514651 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17514651 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17514651 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17514651 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17514651 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17514651 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17514651 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:17514651 | pubmed:issn | 0020-7136 | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:FriedmanScott... | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:ChanAndrew... | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:MisraAnjanA | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:FeuersteinBur... | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:NarlaGouthamG | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:MartignettiJo... | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:TeixeiraMiria... | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:DiFeoAnalisaA | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:Camacho-Vaneg... | lld:pubmed |
| pubmed-article:17514651 | pubmed:author | pubmed-author:SinghGobindG | lld:pubmed |
| pubmed-article:17514651 | pubmed:copyrightInfo | (c) 2007 Wiley-Liss, Inc. | lld:pubmed |
| pubmed-article:17514651 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17514651 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:17514651 | pubmed:volume | 121 | lld:pubmed |
| pubmed-article:17514651 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17514651 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17514651 | pubmed:pagination | 1390-5 | lld:pubmed |
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| pubmed-article:17514651 | pubmed:meshHeading | pubmed-meshheading:17514651... | lld:pubmed |
| pubmed-article:17514651 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17514651 | pubmed:articleTitle | Functional inactivation of the KLF6 tumor suppressor gene by loss of heterozygosity and increased alternative splicing in glioblastoma. | lld:pubmed |
| pubmed-article:17514651 | pubmed:affiliation | Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA. | lld:pubmed |
| pubmed-article:17514651 | pubmed:publicationType | Journal Article | lld:pubmed |
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