Source:http://linkedlifedata.com/resource/pubmed/id/20878114
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rdf:type | |
lifeskim:mentions |
umls-concept:C0006118,
umls-concept:C0017262,
umls-concept:C0018866,
umls-concept:C0037083,
umls-concept:C0037378,
umls-concept:C0042172,
umls-concept:C0086418,
umls-concept:C0185117,
umls-concept:C0443199,
umls-concept:C0449432,
umls-concept:C1179435,
umls-concept:C1524073,
umls-concept:C1548799,
umls-concept:C1705248,
umls-concept:C1710082,
umls-concept:C2911684
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pubmed:issue |
5
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pubmed:dateCreated |
2010-9-29
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pubmed:abstractText |
The hedgehog (Hh) transcription factor Gli induces transformation of epithelial cells via induction of Snail, a repressor of E-cadherin. Epithelial-mesenchymal transition is also a determinant of the progression of tumorigenesis, following down-regulation of E-cadherin. However, the role of Hh signaling components and Snail/E-cadherin in brain tumors is not yet fully understood. We analyzed the expression of Hh signaling components and Snail/E-cadherin in 69 brain tumors by reverse transcription-polymerase chain reaction (RT-PCR). The data showed that overexpression of Smo (35/69), Ptch (50/69), Gli1 (56/69), Gli2 (29/69) and N-myc (39/69) might contribute to brain tumorigenesis. Our results also indicated that Snail and E-cadherin showed opposing expression in malignant tumors (high grade astrocytoma and metastasis). Snail and E-cadherin showed less correlation in benign brain tumors. We further investigated mutations of Gli2 and Snail by RT-PCR and direct sequencing. No mutation was observed on Gli2 but several sporadic mutations on Snail were found, including S96G, S111L, S111L/S119Y and one nonsense mutation at codon 158 (Y158*). An in vitro E-cadherin promoter assay showed that S96G, S111L, S111L/S119Y Snail mutants were decreased by 15, 25 and 50%, respectively, whereas Y158* was increased by 40% compared to wild-type. Furthermore, our data showed that wild-type Snail and S96G, S111L, S111L/S119Y translocated to the nucleus, while the Y158* mutant failed to translocate to the nucleus. Taken together, our results demonstrate that Hh signaling components, the expression and mutations of Snail and the expression of E-cadherin may play an important role in human brain tumorigenesis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1791-2431
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pubmed:author |
pubmed-author:ChangChung-ShingCS,
pubmed-author:ChangLi-KwanLK,
pubmed-author:ChenWei-JayWJ,
pubmed-author:ChioChung-ChingCC,
pubmed-author:ChouChia-HuaCH,
pubmed-author:FuWen-ShaneWS,
pubmed-author:HongYi-RenYR,
pubmed-author:HowngShen-LongSL,
pubmed-author:HsuChing-MeiCM,
pubmed-author:LiaoHuei-DeHD,
pubmed-author:LieuAnn-ShungAS,
pubmed-author:LinChing-ChihCC,
pubmed-author:LinRun-ChinRC,
pubmed-author:LohJoon-KhimJK,
pubmed-author:WuChia-HungCH
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pubmed:issnType |
Electronic
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1225-32
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pubmed:meshHeading |
pubmed-meshheading:20878114-Brain Neoplasms,
pubmed-meshheading:20878114-Cadherins,
pubmed-meshheading:20878114-Down-Regulation,
pubmed-meshheading:20878114-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:20878114-Hedgehog Proteins,
pubmed-meshheading:20878114-Humans,
pubmed-meshheading:20878114-Mutagenesis, Site-Directed,
pubmed-meshheading:20878114-Point Mutation,
pubmed-meshheading:20878114-Promoter Regions, Genetic,
pubmed-meshheading:20878114-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20878114-Signal Transduction,
pubmed-meshheading:20878114-Subcellular Fractions,
pubmed-meshheading:20878114-Transcription Factors
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pubmed:year |
2010
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pubmed:articleTitle |
Differential expression of hedgehog signaling components and Snail/E-cadherin in human brain tumors.
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pubmed:affiliation |
Department of Biochemistry, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan, ROC.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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