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rdf:type |
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lifeskim:mentions |
umls-concept:C0079904,
umls-concept:C0086418,
umls-concept:C0205282,
umls-concept:C0205314,
umls-concept:C0449258,
umls-concept:C0591833,
umls-concept:C0679622,
umls-concept:C1332838,
umls-concept:C1335798,
umls-concept:C1366582,
umls-concept:C1512409
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pubmed:issue |
4
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pubmed:dateCreated |
2009-10-5
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pubmed:abstractText |
The nuclear factor-kappaB (NF-kappaB) signaling pathway has been recently shown to participate in inflammation-induced cancer progression. Here, we describe a detailed analysis of the NF-kappaB-dependent gene regulatory network in the well-established Mdr2 knockout mouse model of inflammation-associated liver carcinogenesis. Expression profiling of NF-kappaB-deficient and NF-kappaB-proficient hepatocellular carcinoma (HCC) revealed a comprehensive list of known and novel putative NF-kappaB target genes, including S100a8 and S100a9. We detected increased co-expression of S100A8 and S100A9 proteins in mouse HCC cells, in human HCC tissue, and in the HCC cell line Hep3B on ectopic RelA expression. Finally, we found a synergistic function for S100A8 and S100A9 in Hep3B cells resulting in a significant induction of reactive oxygen species (ROS), accompanied by enhanced cell survival. CONCLUSION: We identified S100A8 and S100A9 as novel NF-kappaB target genes in HCC cells during inflammation-associated liver carcinogenesis and provide experimental evidence that increased co-expression of both proteins supports malignant progression by activation of ROS-dependent signaling pathways and protection from cell death.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1527-3350
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pubmed:author |
pubmed-author:AngelPeterP,
pubmed-author:Ben-NeriahYinonY,
pubmed-author:BreuhahnKaiK,
pubmed-author:GebhardtChristofferC,
pubmed-author:HaagDanielD,
pubmed-author:HahnMeinhardM,
pubmed-author:HessJochenJ,
pubmed-author:HorwitzEladE,
pubmed-author:LongerichThomasT,
pubmed-author:NémethJuliaJ,
pubmed-author:PikarskyEliE,
pubmed-author:RiehlAstridA,
pubmed-author:SchirmacherPeterP,
pubmed-author:SteinIlanI
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pubmed:issnType |
Electronic
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pubmed:volume |
50
|
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pubmed:owner |
NLM
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|
pubmed:authorsComplete |
Y
|
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pubmed:pagination |
1251-62
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pubmed:meshHeading |
pubmed-meshheading:19670424-Animals,
pubmed-meshheading:19670424-Apoptosis,
pubmed-meshheading:19670424-Calgranulin A,
pubmed-meshheading:19670424-Calgranulin B,
pubmed-meshheading:19670424-Carcinoma, Hepatocellular,
pubmed-meshheading:19670424-Cell Line, Tumor,
pubmed-meshheading:19670424-Disease Models, Animal,
pubmed-meshheading:19670424-Humans,
pubmed-meshheading:19670424-Liver Neoplasms,
pubmed-meshheading:19670424-Mice,
pubmed-meshheading:19670424-Mice, Knockout,
pubmed-meshheading:19670424-Mice, Transgenic,
pubmed-meshheading:19670424-NF-kappa B,
pubmed-meshheading:19670424-P-Glycoproteins,
pubmed-meshheading:19670424-Reactive Oxygen Species,
pubmed-meshheading:19670424-Signal Transduction
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pubmed:year |
2009
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pubmed:articleTitle |
S100A8 and S100A9 are novel nuclear factor kappa B target genes during malignant progression of murine and human liver carcinogenesis.
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pubmed:affiliation |
Division of Signal Transduction and Growth Control (A100), German Cancer Research Center (DKFZ), DKFZ-ZMBH Alliance, Heidelberg, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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