Source:http://linkedlifedata.com/resource/pubmed/id/19082487
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2008-12-16
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pubmed:abstractText |
The mutated K-ras gene is involved in approximately 30% of human cancers. In order to search for K-ras oncogene-induced modulators in lung tissues of K-ras transgenic mice, we performed microarray and proteomics (LC/ESI-MS/MS) analysis. Genes (RAB27b RAS family, IL-1RA, IL-33, chemokine ligand 6, epiregulin, EGF-like domain and cathepsin) related to cancer development (Wnt signaling pathway) and inflammation (chemokine/cytokine signaling pathway, Toll receptor signaling) were up-regulated while genes (troponin, tropomodulin 2, endothelial lipase, FGFR4, integrin alpha8 and adenylate cyclase 8) related to the tumor suppression such as p53 pathway, TGF-beta signaling pathway and cadherin signaling pathway were down-regulated by K-ras oncogene. Proteomics approach revealed that up-regulated proteins in lung adenomas of K-ras mice were classified as follows: proteins related to the metabolism/catabolism (increased from 7 to 22% by K-ras gene), proteins related to translation/transcription and nucleotide (from 4 to 6%), proteins related to signal transduction (from 3 to 5%), proteins related to phosphorylation (from 1 to 2%). ATP synthase, Ras oncogene family, cytochrome c oxidase, flavoprotein, TEF 1, adipoprotein A-1 BP, glutathione oxidase, fatty acid BP 4, diaphorase 1, MAPK4 and transgelin were up-regulated by K-ras oncogene. However, integrin alpha1, Ras-interacting protein (Rain), endothelin-converting enzyme-1d and splicing factor 3b were down-regulated. These studies suggest that genes related to cancer development and inflammation were up-regulated while genes related to the tumor suppression were down-regulated by K-ras, resulting in the tumor growth. Putative biomarkers such as cell cycle related genes (Cdc37), cancer cell adhesion (Glycam 1, integrin alpha8, integrin alphaX and Clec4n), signal transduction (Tlr2, IL-33, and Ccbp2), migration (Ccr1, Ccl6, and diaphorase 1 (Cyb5r3) and cancer development (epiregulin) can be useful for diagnosis and as prognosis markers and some of the target molecules can be applied for prevention of cancer.
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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 |
Jan
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pubmed:issn |
1019-6439
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pubmed:author |
pubmed-author:ChoMinchulM,
pubmed-author:ChoiHeesookH,
pubmed-author:KangGum YongGY,
pubmed-author:KangJungwooJ,
pubmed-author:KimEunjinE,
pubmed-author:KimHeejongH,
pubmed-author:KimJungheeJ,
pubmed-author:KimKwang PyoKP,
pubmed-author:LeeSojungS,
pubmed-author:ParkSue-NieSN,
pubmed-author:ParkYoung-HoYH,
pubmed-author:SeoEunheeE,
pubmed-author:YoonDo-YoungDY,
pubmed-author:YuDae-YeulDY,
pubmed-author:YumYoung NaYN
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pubmed:issnType |
Print
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pubmed:volume |
34
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
161-72
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pubmed:meshHeading |
pubmed-meshheading:19082487-Adenoma,
pubmed-meshheading:19082487-Animals,
pubmed-meshheading:19082487-Electrophoresis, Gel, Two-Dimensional,
pubmed-meshheading:19082487-Gene Expression Profiling,
pubmed-meshheading:19082487-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:19082487-Genes, ras,
pubmed-meshheading:19082487-Humans,
pubmed-meshheading:19082487-Lung Neoplasms,
pubmed-meshheading:19082487-Mice,
pubmed-meshheading:19082487-Mice, Transgenic,
pubmed-meshheading:19082487-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:19082487-Proteomics,
pubmed-meshheading:19082487-Spectrometry, Mass, Matrix-Assisted Laser...,
pubmed-meshheading:19082487-Transcription, Genetic,
pubmed-meshheading:19082487-Tumor Markers, Biological
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pubmed:year |
2009
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pubmed:articleTitle |
Profiling of transcripts and proteins modulated by K-ras oncogene in the lung tissues of K-ras transgenic mice by omics approaches.
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pubmed:affiliation |
Department of Bioscience and Biotechnology, Konkuk University, Gwangjin-gu, Seoul 143-701, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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