Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/40312
DC FieldValueLanguage
dc.contributor.authorYao, P.L.en_US
dc.contributor.author陳健尉zh_TW
dc.contributor.authorLin, Y.C.en_US
dc.contributor.authorWang, C.H.en_US
dc.contributor.authorHuang, Y.C.en_US
dc.contributor.authorLiao, W.Y.en_US
dc.contributor.authorWang, S.S.en_US
dc.contributor.authorChen, J.J.W.en_US
dc.contributor.authorYang, P.C.en_US
dc.date2005zh_TW
dc.date.accessioned2014-06-06T08:03:35Z-
dc.date.available2014-06-06T08:03:35Z-
dc.identifier.issn1044-1549zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/40312-
dc.description.abstractWe had previously demonstrated that lung cancer cells, upon contact with macrophages, could be induced to secrete angiogenic factors to promote tumor angiogenesis. In this study, we focused on the paracrine and autocrine regulation of interleukin (IL)-8 expression in sensitized lung cancer cells after interacting with macrophages. We found that the IL-8 mRNA expression in lung cancer cells significantly increased after coculture with phorbol myristate acetate-treated THP-1 cells and human primary lung macrophages. Fresh lung cancer CL1-5 cells cocultured with macrophage-sensitized lung cancer cells still had a 35 % of increase in IL-8 mRNA expression. The addition of anti-inflammatory agents pyrrolidine dithiocarbamate, pentoxifylline, aspirin, and dexamethasone could completely suppress the expression of IL-8 mRNA in fresh/sensitized lung cancer cell cocultures. Human recombinant tumor necrosis factor (TNF)-α and IL-1α could induce IL-8 expression in lung cancer cells in a dose-dependent manner. Neutralization with TNF-α and IL-1α antibodies in cocultures decreased the levels of IL-8 expression in sensitized lung cancer cells. Nuclear factor-κ B transcriptional activity was also suppressed by the same antibodies, as confirmed by a reporter gene assay and the electrophoretic mobility shift assay. Our results highly suggest that both autocrine and paracrine regulation are involved in IL-8 expression of lung cancer cells cocultured with macrophage. Also, the regulations of IL-8 expression in lung cancer cells were through the nuclear factor-κ B pathway and modulated by TNF-α and IL-1α.en_US
dc.language.isoen_USzh_TW
dc.relationAmerican Journal of Respiratory Cell and Molecular Biologyen_US
dc.relation.ispartofseriesAmerican Journal of Respiratory Cell and Molecular Biology, Volume 32, Issue 6, Page(s) 540-547.en_US
dc.relation.urihttp://dx.doi.org/10.1165/rcmb.2004-0223OCen_US
dc.subjectautocrineen_US
dc.subjectinflammationen_US
dc.subjectlung canceren_US
dc.subjectmacrophagesen_US
dc.subjectNF-kappa Ben_US
dc.subjectendothelial growth-factoren_US
dc.subjectnecrosis-factor-alphaen_US
dc.subjectfactor-kappa-ben_US
dc.subjecttumoren_US
dc.subjectangiogenesisen_US
dc.subjectgene-expressionen_US
dc.subjectpatient survivalen_US
dc.subjectepithelial-cellsen_US
dc.subjectmacrophage infiltrationen_US
dc.subjectalveolar macrophagesen_US
dc.subjectmessenger-rnaen_US
dc.titleAutocrine and paracrine regulation of interleukin-8 expression in lung cancer cellsen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1165/rcmb.2004-0223OCzh_TW
item.grantfulltextnone-
item.fulltextno fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en_US-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
Appears in Collections:生物醫學研究所
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