Abstract
The processes by which cancer cells leave the tumor and enter adjacent tissue is known as invasion, whereas metastasis refers to secondary tumor colonization of tissue at a distance from the primary lesion. These two events are the most lethal of cancer phenomena and the signaling mechanisms that govern them are complex. The Ras signaling pathways are well represented in their involvement in tumor initiation, but considerably less is known about their contribution to invasion and metastasis. In this review, we discuss the current evidence for mutant Ras proteins as significant players in these aspects of cancer progression.
MeSH terms
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Actins / metabolism
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Animals
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Cell Adhesion / genetics
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Extracellular Matrix / metabolism
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Gene Expression Regulation
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Humans
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Mice
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Mitogen-Activated Protein Kinases / metabolism
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Monomeric GTP-Binding Proteins / metabolism
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Neoplasm Invasiveness* / genetics
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Neoplasm Metastasis* / genetics
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Neovascularization, Pathologic / metabolism
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Oncogene Protein p21(ras) / genetics
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Oncogene Protein p21(ras) / metabolism
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Oncogene Protein p21(ras) / physiology*
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Phosphatidylinositol 3-Kinases / metabolism
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Proteins / metabolism
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Proto-Oncogene Proteins c-met
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Proto-Oncogene Proteins*
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Receptors, Growth Factor*
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Response Elements / genetics
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Signal Transduction
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rho GTP-Binding Proteins / metabolism
Substances
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Actins
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Proteins
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Proto-Oncogene Proteins
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Receptors, Growth Factor
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Phosphatidylinositol 3-Kinases
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MET protein, human
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Proto-Oncogene Proteins c-met
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Mitogen-Activated Protein Kinases
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Monomeric GTP-Binding Proteins
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Oncogene Protein p21(ras)
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rho GTP-Binding Proteins