Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/40335
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dc.contributor.authorChen, J.J.W.en_US
dc.contributor.author陳健尉zh_TW
dc.contributor.authorYao, P.L.en_US
dc.contributor.authorYuan, A.en_US
dc.contributor.authorHong, T.M.en_US
dc.contributor.authorShun, C.T.en_US
dc.contributor.authorKuo, M.L.en_US
dc.contributor.authorLee, Y.C.en_US
dc.contributor.authorYang, P.C.en_US
dc.date2003zh_TW
dc.date.accessioned2014-06-06T08:03:37Z-
dc.date.available2014-06-06T08:03:37Z-
dc.identifier.issn1078-0432zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/40335-
dc.description.abstractPurpose: To evaluate the interaction between tumor-infiltrating macrophages and cancer cells and its effect on the expression of a potent angiogenic factor, interleukin-8 (IL-8), tumor angiogenesis, and patient outcome in non-small cell lung cancer (NSCLC). Experimental Design: We measured tumor IL-8 mRNA expression (by real-time quantitative reverse transcription-PCR), intratumor microvessel counts, and tumor-infiltrating macrophage density (by immunohistochemical staining) in 35 NSCLC surgical specimens and correlated with the patient's clinical outcome. We then investigated the interaction between macrophages (cell line THP-1) and six different human cancer cell lines (four NSCLCs, one osteosarcoma, and one hepatoma) and its effect on IL-8 mRNA expression using a macrophage/cancer cell coculture system, IL-8 mRNA expression in lung cancer cells, and macrophages being measured separately after coculture in the presence or absence of six anti-inflammatory agents, i.e., pentoxifylline, aspirin, indomethacin, dexamethasone, celecoxib (a selective cyclooxygenase-2 inhibitor), and pyrrolidine dithiocarbamate, a specific nuclear factor kappaB (NF-kappaB) inhibitor. NF-kappaB transcriptional activity and protein levels were measured by reporter gene assay and Western blot. Results: The tumor-infiltrating macrophage density correlated significantly and positively with tumor IL-8 mRNA expression and intratumor microvessel counts and significantly and negatively with patient survival. In addition, after cell-cell interaction in cancer cell:macrophage cocultures, marked IL-8 mRNA expression was induced in lung cancer cells (similar to270-fold) and, to a lesser degree, in macrophages (4.5-fold). The increase in IL-8 mRNA expression correlated with the in vitro metastatic potential of the cancer cells. All six anti-inflammatory agents suppressed induction of IL-8 mRNA expression in lung cancer cells by >90%, four (pentoxifylline, celecoxib, pyrrolidine dithiocarbamate, and dexamethasone) having a dose-dependent effect. NF-kappaB transcriptional regulation and protein levels were simultaneously increased in the nuclei of cancer cells in macrophage/cancer cell cocultures, this effect also being suppressed by all six anti-inflammatory agents. Conclusions: The interaction between infiltrating macrophages and cancer cells up-regulates IL-8 mRNA expression, especially in the cancer cells; this may contribute greatly to the increased tumor angiogenesis and adverse outcome in NSCLC patients with a high density of tumor-infiltrating macrophages. Anti-inflammatory agents can suppress the induction of IL-8 mRNA expression seen in lung cancer cells after coculture with macrophages, and this suppression is mediated, in part, through the NF-kappaB pathway.en_US
dc.language.isoen_USzh_TW
dc.relationClinical Cancer Researchen_US
dc.relation.ispartofseriesClinical Cancer Research, Volume 9, Issue 2, Page(s) 729-737.en_US
dc.subjectinvasive breast-carcinomaen_US
dc.subjecthuman prostate-canceren_US
dc.subjecthuman-melanoma cellsen_US
dc.subjectkappa-ben_US
dc.subjectcolorectal-canceren_US
dc.subjectepithelial-cellsen_US
dc.subjectgrowth-factoren_US
dc.subjectclinical-applicationsen_US
dc.subjectpossible involvementen_US
dc.subjectmicrovessel densityen_US
dc.titleUp-regulation of tumor interleukin-8 expression by infiltrating macrophages: Its correlation with tumor angiogenesis and patient survival in non-small cell lung canceren_US
dc.typeJournal Articlezh_TW
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en_US-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.fulltextno fulltext-
item.cerifentitytypePublications-
Appears in Collections:生物醫學研究所
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