DC Field | Value | Language |
---|---|---|
dc.contributor.author | Park, HD | ko |
dc.contributor.author | Lee, Y | ko |
dc.contributor.author | Oh, YK | ko |
dc.contributor.author | Jung, JG | ko |
dc.contributor.author | Park, YW | ko |
dc.contributor.author | Myung, K | ko |
dc.contributor.author | Kim, KH | ko |
dc.contributor.author | Koh, SS | ko |
dc.contributor.author | Lim, Dae-Sik | ko |
dc.date.accessioned | 2013-04-29T01:02:51Z | - |
dc.date.available | 2013-04-29T01:02:51Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2011-01 | - |
dc.identifier.citation | ONCOGENE, v.30, no.2, pp.201 - 211 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | http://hdl.handle.net/10203/173629 | - |
dc.description.abstract | Pancreatic adenocarcinoma upregulated factor (PAUF) is overproduced in certain types of cancer. However, little is known of the tumorigenic function of PAUF. In this study, we report the X-ray crystal structure of PAUF and reveal that PAUF is a mammalian lectin normally found in plant lectins. We also identify PAUF as an endogenous ligand of Toll-like receptor 2 (TLR2) and TLR4 by screening extracellular domain receptor pools. We further confirmed the specificity of the PAUF-TLR2 interaction. PAUF induces extracellular signal-regulated kinase (ERK) phosphorylation and activates the IKK-beta-mediated TPL2/MEK/ERK signaling pathway through TLR2. In agreement with the result of TLR2-mediated ERK activation by PAUF, PAUF induces increased expression of the protumorigenic cytokines RANTES and MIF in THP-1 cells. However, PAUF does not fully activate I kappa-B-alpha signaling pathways in THP-1 cells, and fails to translocate the p65 subunit of the nuclear factor-kappa B (NF-kappa B) complex into the nucleus, resulting in no NF-kappa B activation. Surprisingly, we found that PAUF also associated with the CXC chemokine receptor (CXCR4)-TLR2 complex and inhibited CXCR4-dependent, TLR2-mediated NF-kappa B activation. Together, these findings suggest that the new cancer-associated ligand, PAUF, may activate TLR-mediated ERK signaling to produce the protumorigenic cytokines, but inhibits TLR-mediated NF-kappa B signaling, thereby facilitating tumor growth and escape from innate immune surveillance. Oncogene (2011) 30, 201-211; doi:10.1038/onc.2010.401; published online 30 August 2010 | - |
dc.language | English | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.title | Pancreatic adenocarcinoma upregulated factor promotes metastasis by regulating TLR/CXCR4 activation | - |
dc.type | Article | - |
dc.identifier.wosid | 000286438900008 | - |
dc.identifier.scopusid | 2-s2.0-78651407343 | - |
dc.type.rims | ART | - |
dc.citation.volume | 30 | - |
dc.citation.issue | 2 | - |
dc.citation.beginningpage | 201 | - |
dc.citation.endingpage | 211 | - |
dc.citation.publicationname | ONCOGENE | - |
dc.identifier.doi | 10.1038/onc.2010.401 | - |
dc.contributor.localauthor | Lim, Dae-Sik | - |
dc.contributor.nonIdAuthor | Park, HD | - |
dc.contributor.nonIdAuthor | Lee, Y | - |
dc.contributor.nonIdAuthor | Oh, YK | - |
dc.contributor.nonIdAuthor | Jung, JG | - |
dc.contributor.nonIdAuthor | Park, YW | - |
dc.contributor.nonIdAuthor | Myung, K | - |
dc.contributor.nonIdAuthor | Kim, KH | - |
dc.contributor.nonIdAuthor | Koh, SS | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | PAUF | - |
dc.subject.keywordAuthor | TLR | - |
dc.subject.keywordAuthor | CXCR4 | - |
dc.subject.keywordAuthor | TPL2 | - |
dc.subject.keywordAuthor | ERK | - |
dc.subject.keywordAuthor | NF-kappa B | - |
dc.subject.keywordPlus | TOLL-LIKE RECEPTORS | - |
dc.subject.keywordPlus | TUMOR-GROWTH | - |
dc.subject.keywordPlus | CARBOHYDRATE SPECIFICITIES | - |
dc.subject.keywordPlus | STRUCTURAL BASIS | - |
dc.subject.keywordPlus | BINDING LECTINS | - |
dc.subject.keywordPlus | CANCER-CELLS | - |
dc.subject.keywordPlus | ANGIOGENESIS | - |
dc.subject.keywordPlus | LIPOPOLYSACCHARIDE | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | PROGRESSION | - |
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