| pubmed-article:12543789 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12543789 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:12543789 | lifeskim:mentions | umls-concept:C0037657 | lld:lifeskim |
| pubmed-article:12543789 | lifeskim:mentions | umls-concept:C0031621 | lld:lifeskim |
| pubmed-article:12543789 | lifeskim:mentions | umls-concept:C1545588 | lld:lifeskim |
| pubmed-article:12543789 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
| pubmed-article:12543789 | lifeskim:mentions | umls-concept:C0332291 | lld:lifeskim |
| pubmed-article:12543789 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12543789 | pubmed:dateCreated | 2003-1-24 | lld:pubmed |
| pubmed-article:12543789 | pubmed:abstractText | The mTOR inhibitor rapamycin induces G1 cell cycle accumulation and p53-independent apoptosis of the human rhabdomyosarcoma cell line Rh1. Insulin-like growth factor I (IGF-I) and insulin, but not epidermal growth factor or platelet-derived growth factor, completely prevented apoptosis of this cell line. Because the Ras-Erk1-Erk2 and phosphatidylinositol 3'-kinase (PI3K)-Akt pathways are implicated in the survival of various cancer cells, we determined whether protection from rapamycin-induced apoptosis by IGF-I requires one or both of these pathways. Despite the blocking of Ras-Erk signaling by the addition of PD 98059 (a MEK1 inhibitor) or by the overexpression of dominant-negative RasN17, IGF-I completely prevented rapamycin-induced death. Inhibition of Ras signaling did not prevent Akt activation by IGF-I. To determine the role of the PI3K-Akt pathway in rescuing cells from apoptosis caused by rapamycin, cells expressing dominant-negative Akt were tested. This mutant protein inhibited IGF-I-induced phosphorylation of Akt and blocked phosphorylation of glycogen synthase kinase 3. The prevention of rapamycin-induced apoptosis by IGF-I was not inhibited by expression of dominant-negative Akt either alone or under conditions in which LY 294002 inhibited PI3K signaling. Furthermore, IGF-I prevented rapamycin-induced apoptosis when the Ras-Erk1-Erk2 and PI3K-Akt pathways were blocked simultaneously. Similar experiments in a second rhabdomyosarcoma cell line, Rh30, using pharmacological inhibitors of PI3K or MEK1, alone or in combination, failed to block IGF-I rescue from rapamycin-induced apoptosis. Therefore, we conclude that a novel pathway(s) is responsible for the IGF-I-mediated protection against rapamycin-induced apoptosis in these rhabdomyosarcoma cells. | lld:pubmed |
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| pubmed-article:12543789 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12543789 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12543789 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12543789 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12543789 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:12543789 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:12543789 | pubmed:author | pubmed-author:HoughtonPeter... | lld:pubmed |
| pubmed-article:12543789 | pubmed:author | pubmed-author:GermainGlen... | lld:pubmed |
| pubmed-article:12543789 | pubmed:author | pubmed-author:HarwoodFrankl... | lld:pubmed |
| pubmed-article:12543789 | pubmed:author | pubmed-author:ThimmaiahKunt... | lld:pubmed |
| pubmed-article:12543789 | pubmed:author | pubmed-author:HuangShileS | lld:pubmed |
| pubmed-article:12543789 | pubmed:author | pubmed-author:EastonJohnJ | lld:pubmed |
| pubmed-article:12543789 | pubmed:author | pubmed-author:VeverkaKaren... | lld:pubmed |
| pubmed-article:12543789 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12543789 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:12543789 | pubmed:volume | 63 | lld:pubmed |
| pubmed-article:12543789 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12543789 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12543789 | pubmed:pagination | 364-74 | lld:pubmed |
| pubmed-article:12543789 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:12543789 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12543789 | pubmed:articleTitle | Insulin-like growth factor I-mediated protection from rapamycin-induced apoptosis is independent of Ras-Erk1-Erk2 and phosphatidylinositol 3'-kinase-Akt signaling pathways. | lld:pubmed |
| pubmed-article:12543789 | pubmed:affiliation | Department of Molecular Pharmacology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794, USA. | lld:pubmed |
| pubmed-article:12543789 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12543789 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12543789 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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