pubmed-article:17384145 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C0034802 | lld:lifeskim |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C0007137 | lld:lifeskim |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C0040624 | lld:lifeskim |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C1366765 | lld:lifeskim |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C1422733 | lld:lifeskim |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:17384145 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:17384145 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:17384145 | pubmed:dateCreated | 2007-8-1 | lld:pubmed |
pubmed-article:17384145 | pubmed:abstractText | In squamous cell carcinoma, the levels of nitric oxide (NO) derived from inducible NO synthase (iNOS) and prostaglandin E2 (PGE2) derived from cyclooxygenase-2 (COX-2) originated from tumor cells or tumor-associated inflammatory cells have been reported to correlate with tumor growth, metastasis, and angiogenesis. The present study examined the role of the iNOS signaling pathway in PGE2-mediated tumor invasiveness and proliferation in squamous cell carcinoma, A431, and SCC-9 cells. Cell invasion and proliferation promoted by PGE2 were blocked by iNOS silencing RNA or iNOS/guanylate cyclase (GC) pharmacological inhibition. Consistently, iNOS-GC pathway inhibitors blocked mitogen-activated protein kinase-ERK1/2 phosphorylation, which was required to mediate PGE2 functions. In vivo, in A431 cells implanted in nude mice, GC inhibition also decreased the tumor proliferation index and ERK1/2 activation. PGE2 effects were confined to the selective stimulation of the EP2 receptor subtype, leading to epidermal growth factor receptor (EGFR) transactivation via protein kinase A (PKA) and c-Src activation. EP2-mediated ERK1/2 activation and cell functions were abolished by inhibitors of PKA, c-Src, and EGFR, as well as by inhibiting iNOS pathway. Silencing of iNOS also impaired EGFR-induced ERK1/2 phosphorylation. These results indicate that iNOS/GC signaling is a downstream player in the control of EP2/EGFR-mediated tumor cell proliferation and invasion. | lld:pubmed |
pubmed-article:17384145 | pubmed:language | eng | lld:pubmed |
pubmed-article:17384145 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17384145 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17384145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17384145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17384145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17384145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17384145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17384145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17384145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17384145 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17384145 | pubmed:month | Aug | lld:pubmed |
pubmed-article:17384145 | pubmed:issn | 1530-6860 | lld:pubmed |
pubmed-article:17384145 | pubmed:author | pubmed-author:MorbidelliLuc... | lld:pubmed |
pubmed-article:17384145 | pubmed:author | pubmed-author:ZicheMarinaM | lld:pubmed |
pubmed-article:17384145 | pubmed:author | pubmed-author:DonniniSandra... | lld:pubmed |
pubmed-article:17384145 | pubmed:author | pubmed-author:SolitoRaffael... | lld:pubmed |
pubmed-article:17384145 | pubmed:author | pubmed-author:SacchettiAndr... | lld:pubmed |
pubmed-article:17384145 | pubmed:author | pubmed-author:PatrignaniPao... | lld:pubmed |
pubmed-article:17384145 | pubmed:author | pubmed-author:FinettiFederi... | lld:pubmed |
pubmed-article:17384145 | pubmed:author | pubmed-author:TerzuoliErika... | lld:pubmed |
pubmed-article:17384145 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17384145 | pubmed:volume | 21 | lld:pubmed |
pubmed-article:17384145 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17384145 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17384145 | pubmed:pagination | 2418-30 | lld:pubmed |
pubmed-article:17384145 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:17384145 | pubmed:meshHeading | pubmed-meshheading:17384145... | lld:pubmed |
pubmed-article:17384145 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17384145 | pubmed:articleTitle | EP2 prostanoid receptor promotes squamous cell carcinoma growth through epidermal growth factor receptor transactivation and iNOS and ERK1/2 pathways. | lld:pubmed |
pubmed-article:17384145 | pubmed:affiliation | Department of Molecular Biology, Pharmacology Angiogenesis Lab., University of Siena, Via Aldo Moro, 2, 53100, Siena, Italy. | lld:pubmed |
pubmed-article:17384145 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17384145 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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