| pubmed-article:8692920 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8692920 | lifeskim:mentions | umls-concept:C0014597 | lld:lifeskim |
| pubmed-article:8692920 | lifeskim:mentions | umls-concept:C1706586 | lld:lifeskim |
| pubmed-article:8692920 | lifeskim:mentions | umls-concept:C1510411 | lld:lifeskim |
| pubmed-article:8692920 | lifeskim:mentions | umls-concept:C0812215 | lld:lifeskim |
| pubmed-article:8692920 | lifeskim:mentions | umls-concept:C2746015 | lld:lifeskim |
| pubmed-article:8692920 | lifeskim:mentions | umls-concept:C0752319 | lld:lifeskim |
| pubmed-article:8692920 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:8692920 | lifeskim:mentions | umls-concept:C0205410 | lld:lifeskim |
| pubmed-article:8692920 | pubmed:issue | 14 | lld:pubmed |
| pubmed-article:8692920 | pubmed:dateCreated | 1996-8-29 | lld:pubmed |
| pubmed-article:8692920 | pubmed:abstractText | The potent transforming activity of membrane-targeted Raf-1 (Raf-CAAX) suggests that Ras transformation is triggered primarily by a Ras-mediated translocation of Raf-1 to the plasma membrane. However, whereas constitutively activated mutants of Ras [H-Ras(61L) and K-Ras4B(12V)] and Raf-1 (DeltaRaf-22W and Raf-CAAX) caused indistinguishable morphologic and growth (in soft agar and nude mice) transformation of NIH 3T3 fibroblasts, only mutant Ras caused morphologic transformation of RIE-1 rat intestinal cells. Furthermore, only mutant Ras-expressing RIE-1 cells formed colonies in soft agar and developed rapid and progressive tumors in nude mice. We also observed that activated Ras, but not Raf-1, caused transformation of IEC-6 rat intestinal and MCF-10A human mammary epithelial cells. Although both Ras- and DeltaRaf-22W-expressing RIE-1 cells showed elevated Raf-1 and mitogen-activated protein (MAP) kinase activities, only Ras-transformed cells produced secreted factors that promoted RIE-1 transformation. Incubation of untransformed RIE-1 cells in the presence of conditioned medium from Ras-expressing, but not DeltaRaf-22W-expressing, cells caused a rapid and stable morphologic transformation that was indistinguishable from the morphology of Ras-transformed RIE-1 cells. Thus, induction of an autocrine growth mechanism may distinguish the transforming actions of Ras and Raf. In summary, our observations demonstrate that oncogenic Ras activation of the Raf/MAP kinase pathway alone is not sufficient for full tumorigenic transformation of RIE-1 epithelial cells. Thus, Raf-independent signaling events are essential for oncogenic Ras transformation of epithelial cells, but not fibroblasts. | lld:pubmed |
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| pubmed-article:8692920 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:8692920 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8692920 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8692920 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:8692920 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:8692920 | pubmed:author | pubmed-author:DerC JCJ | lld:pubmed |
| pubmed-article:8692920 | pubmed:author | pubmed-author:ClarkG JGJ | lld:pubmed |
| pubmed-article:8692920 | pubmed:author | pubmed-author:CoffeyR JRJJr | lld:pubmed |
| pubmed-article:8692920 | pubmed:author | pubmed-author:GangarosaL... | lld:pubmed |
| pubmed-article:8692920 | pubmed:author | pubmed-author:OldhamS MSM | lld:pubmed |
| pubmed-article:8692920 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8692920 | pubmed:day | 9 | lld:pubmed |
| pubmed-article:8692920 | pubmed:volume | 93 | lld:pubmed |
| pubmed-article:8692920 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8692920 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8692920 | pubmed:pagination | 6924-8 | lld:pubmed |
| pubmed-article:8692920 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:8692920 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8692920 | pubmed:articleTitle | Activation of the Raf-1/MAP kinase cascade is not sufficient for Ras transformation of RIE-1 epithelial cells. | lld:pubmed |
| pubmed-article:8692920 | pubmed:affiliation | Department of Pharmacology, University of North Carolina, Chapel Hill 27599, USA. | lld:pubmed |
| pubmed-article:8692920 | pubmed:publicationType | Journal Article | lld:pubmed |
