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PMID: 8420573 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

Ras-responsive genes and tumor metastasis.

Critical reviews in oncogenesis ·Vol. 4 ·No. 2 ·1993-00-00 ·Pages 95-114

Chambers AF, Tuck AB

Abstract

Transfected ras oncogenes have been shown to induce metastatic properties in some cells. Clarification of the mechanisms by which ras is able to increase the metastatic ability in model systems will improve our understanding of tumor progression to metastasis, even in those cells in which ras activation has not been implicated. Many of the consequences of ras expression also have been detected in cells that have become metastatic in the apparent absence of an altered ras gene, suggesting that there is a set of common changes that can lead to metastasis with multiple signals capable of eliciting these changes. These changes, which have been documented for some ras-transformed cells, include increased expression or activity of various degradative enzymes, including metalloproteinases (type IV collagenases) and cysteine proteinases (cathepsins L and B), as well as decreased expression or activity of their inhibitors (TIMPs and cystatins, respectively). In addition, some metastatic ras-transformed cells have an increased expression of calcyclin, a cytoplasmic calcium-binding protein, and osteopontin, a secreted calcium-binding protein with possible adhesive function. Not all cells, however, respond in the same fashion to a ras oncogene signal. Some cells are resistant to ras-mediated tumor progression to metastasis. Understanding the mechanism by which these cells fail to respond to a specific oncogene signal may provide clues with broader applicability and potential therapeutic relevance. In this review, we summarize some of the studies in which ras has been used as a tool to learn about the molecular requirements for metastasis. We discuss ras-mediated changes in gene expression and how these may contribute to metastatic ability, as well as some possible mechanisms by which ras expression may result in altered expression of other genes. We also consider some cell lines which appear to be resistant to an oncogenic ras signal and possible mechanisms for this nonresponsiveness. These studies are providing insights into the molecular mechanisms of tumor metastasis and the responses of cells to oncogenic signals.

Related Genes
MeSH Terms
3T3 Cells Animals Calcium-Binding Proteins/genetics,metabolism Cell Cycle Proteins Cell Transformation, Neoplastic Endopeptidases/metabolism Gene Expression Regulation, Neoplastic Genes, ras Humans Mice Neoplasm Metastasis/genetics Oligopeptides/physiology Oncogenes Osteopontin Protease Inhibitors/metabolism S100 Calcium Binding Protein A6 S100 Proteins Sialoglycoproteins/genetics,metabolism Transfection
Chemicals
Calcium-Binding Proteins Cell Cycle Proteins Oligopeptides Protease Inhibitors S100 Calcium Binding Protein A6 S100 Proteins S100a6 protein, mouse SPP1 protein, human Sialoglycoproteins Spp1 protein, mouse S100A6 protein, human Osteopontin glycyl-arginyl-glycyl-aspartyl-serine Endopeptidases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Chambers A F
London Regional Cancer Centre, Ontario, Canada.
Tuck A B
Article Info
Journal
Critical reviews in oncogenesis
Abbr.
Crit Rev Oncog
ISSN
0893-9675
Published
1993-00-00
Pages
95-114
Language
English
Region
United States
NLM ID
8914610
Subset
IM
External Links
PubMed source
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