| pubmed-article:14707447 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14707447 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:14707447 | lifeskim:mentions | umls-concept:C0346647 | lld:lifeskim |
| pubmed-article:14707447 | lifeskim:mentions | umls-concept:C0020349 | lld:lifeskim |
| pubmed-article:14707447 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:14707447 | lifeskim:mentions | umls-concept:C0439064 | lld:lifeskim |
| pubmed-article:14707447 | lifeskim:mentions | umls-concept:C0037080 | lld:lifeskim |
| pubmed-article:14707447 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:14707447 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:14707447 | pubmed:dateCreated | 2004-1-6 | lld:pubmed |
| pubmed-article:14707447 | pubmed:abstractText | Pancreatic carcinoma is characterized by poor prognosis and lack of response to conventional therapy. The reasons for this are not fully understood. We have reported that inhibition of 5-lipoxygenase abolished proliferation and induced apoptosis in pancreatic cancer cells while the 5-lipoxygenase metabolite, 5(S)-hydroxyeicosatetraenoic acid [5(S)-HETE] stimulated pancreatic cancer cell proliferation. The current study was designed to investigate the underlying mechanisms for 5(S)-HETE-stimulated proliferation of pancreatic cells. Two human pancreatic cancer cell lines, PANC-1 and HPAF, were used. Cell proliferation was monitored by thymidine incorporation and cell counting. Phosphorylation of P42/44(MAPK) (mitogen activated protein kinase, ERK), MEK (MAPK/ERK kinase), P38 kinase, JNK/SAPK (c-Jun N-terminal kinase/ stress-activated protein kinase), AKT and tyrosine residues of intracellular proteins was measured by Western blot using their corresponding phospho-specific antibodies. The results showed that (1) 5(S)-HETE markedly stimulated pancreatic cancer cell proliferation in a time- and concentration-dependent manner; (2) 5(S)-HETE induced tyrosine phosphorylation of multiple intracellular proteins while the tyrosine kinase inhibitor, genestein, blocked 5(S)-HETE-stimulated cell proliferation; (3) 5(S)-HETE significantly stimulated both MEK and P42/44(MAPK) phosphorylation and the MEK inhibitors, PD098059 and U0126, inhibited 5(S)-HETE-stimulated proliferation in these two cell lines; (4) 5(S)-HETE also stimulated P38 kinase phosphorylation but the P38 inhibitor, SB203580, did not effect 5(S)-HETE-stimulated cell proliferation; (5) 5(S)-HETE markedly stimulated AKT phosphorylation while the phosphatidylinositide-3 (PI3)-kinase inhibitor, wortmannin, blocked 5(S)-HETE-stimulated cell proliferation; (6) phosphorylation of JNK/SAPK was not induced by 5(S)-HETE, and (7) the general protein kinase C (PKC) inhibitor, GF109203X, did not affect 5(S)-HETE-stimulated cancer cell proliferation. These findings suggest that intracellular tyrosine kinases, MEK/ERK and PI3 kinase/AKT pathways are involved in 5(S)-HETE-stimulated pancreatic cancer cell proliferation but P38 kinase, JNK/SAPK and PKC are not involved in this mitogenic effect. | lld:pubmed |
| pubmed-article:14707447 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14707447 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14707447 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14707447 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14707447 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14707447 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:14707447 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14707447 | pubmed:issn | 0030-2414 | lld:pubmed |
| pubmed-article:14707447 | pubmed:author | pubmed-author:AdrianThomas... | lld:pubmed |
| pubmed-article:14707447 | pubmed:author | pubmed-author:DingXian-Zhon... | lld:pubmed |
| pubmed-article:14707447 | pubmed:author | pubmed-author:TongWei-GangW... | lld:pubmed |
| pubmed-article:14707447 | pubmed:copyrightInfo | Copyright 2003 S. Karger AG, Basel | lld:pubmed |
| pubmed-article:14707447 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14707447 | pubmed:volume | 65 | lld:pubmed |
| pubmed-article:14707447 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14707447 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14707447 | pubmed:pagination | 285-94 | lld:pubmed |
| pubmed-article:14707447 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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| pubmed-article:14707447 | pubmed:meshHeading | pubmed-meshheading:14707447... | lld:pubmed |
| pubmed-article:14707447 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:14707447 | pubmed:articleTitle | Multiple signal pathways are involved in the mitogenic effect of 5(S)-HETE in human pancreatic cancer. | lld:pubmed |
| pubmed-article:14707447 | pubmed:affiliation | Department of Surgery, Northwestern University Medical School, Chicago, Il 60611, USA. | lld:pubmed |
| pubmed-article:14707447 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14707447 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:14707447 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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