pubmed-article:12632066 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12632066 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
pubmed-article:12632066 | lifeskim:mentions | umls-concept:C0346647 | lld:lifeskim |
pubmed-article:12632066 | lifeskim:mentions | umls-concept:C0079633 | lld:lifeskim |
pubmed-article:12632066 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:12632066 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
pubmed-article:12632066 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:12632066 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:12632066 | pubmed:dateCreated | 2003-3-12 | lld:pubmed |
pubmed-article:12632066 | pubmed:abstractText | The purpose of the present study was to examine the expression of interleukin (IL)-8 and IL-8 receptors and to evaluate the effects of IL-8 on human pancreatic cancer. We examined the expression of IL-8 and its two receptors (CXCR1 and CXCR2) in 40 surgically resected human pancreatic cancer tissues and in three different human pancreatic cancer cell lines (PANC-1, MIAPaCa-2 and Capan-2). The immunohistochemical analysis using specific antibodies demonstrated that positive staining for IL-8, CXCR1 and CXCR2 in surgically resected human pancreatic cancer was 50, 55 and 65%, respectively. Moreover, 40% of these cases were positive for both IL-8 and IL-8 receptors. In contrast, immunoreactive signals for those proteins were extremely suppressed in normal pancreatic tissues. All of the pancreatic cancer cell lines expressed IL-8 and IL-8 receptors at the RNA and protein levels. Receptor binding experiments using 125I-labeled IL-8 showed that PANC-1 cells had specific binding sites for IL-8. The cell proliferation assay demonstrated that IL-8 did not affect the growth of the three cell lines. However, treatment with IL-8 enhanced the invasiveness into Matrigel and increased the activity of matrix metalloproteinase (MMP)-2 in supernatants of the PANC-1 cells. These results demonstrate that IL-8 and IL-8 receptors are over-expressed in pancreatic cancer, and suggest that IL-8 regulates MMP-2 activity and plays an important role in the invasiveness of human pancreatic cancer. | lld:pubmed |
pubmed-article:12632066 | pubmed:language | eng | lld:pubmed |
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pubmed-article:12632066 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12632066 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12632066 | pubmed:month | Apr | lld:pubmed |
pubmed-article:12632066 | pubmed:issn | 1019-6439 | lld:pubmed |
pubmed-article:12632066 | pubmed:author | pubmed-author:KitadaiYasuhi... | lld:pubmed |
pubmed-article:12632066 | pubmed:author | pubmed-author:ChayamaKazuak... | lld:pubmed |
pubmed-article:12632066 | pubmed:author | pubmed-author:MukaidaNaofum... | lld:pubmed |
pubmed-article:12632066 | pubmed:author | pubmed-author:SasakiTamitoT | lld:pubmed |
pubmed-article:12632066 | pubmed:author | pubmed-author:KuwadaYukioY | lld:pubmed |
pubmed-article:12632066 | pubmed:author | pubmed-author:MorinakaKenji... | lld:pubmed |
pubmed-article:12632066 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12632066 | pubmed:volume | 22 | lld:pubmed |
pubmed-article:12632066 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12632066 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12632066 | pubmed:pagination | 765-71 | lld:pubmed |
pubmed-article:12632066 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:12632066 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12632066 | pubmed:articleTitle | Potential involvement of IL-8 and its receptors in the invasiveness of pancreatic cancer cells. | lld:pubmed |
pubmed-article:12632066 | pubmed:affiliation | Department of Medicine and Molecular Science, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima 734-8551, Japan. ykuwada@hiroshima-u.ac.jp | lld:pubmed |
pubmed-article:12632066 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12632066 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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