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The transcription factor EGR1 regulates metastatic potential of v-src transformed sarcoma cells
V. Cermák, J. Kosla, J. Plachý, K. Trejbalová, J. Hejnar, M. Dvorák,
Language English Country Switzerland
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
PubMed Central
from 1997
ProQuest Central
from 1997-01-01 to 1 year ago
Medline Complete (EBSCOhost)
from 2000-01-01 to 1 year ago
Health & Medicine (ProQuest)
from 1997-01-01 to 1 year ago
- MeSH
- Cell Adhesion MeSH
- Cell Line MeSH
- Cytoskeleton metabolism MeSH
- Phenotype MeSH
- Kinetics MeSH
- Chickens MeSH
- Neoplasm Metastasis genetics MeSH
- Cell Transformation, Neoplastic genetics pathology MeSH
- Oncogene Protein pp60(v-src) genetics metabolism MeSH
- Cell Movement MeSH
- Cell Proliferation MeSH
- Early Growth Response Protein 1 genetics metabolism MeSH
- Gene Expression Regulation, Neoplastic MeSH
- Sarcoma genetics pathology MeSH
- Gene Expression Profiling MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Metastatic spreading of cancer cells is a highly complex process directed primarily by the interplay between tumor microenvironment, cell surface receptors, and actin cytoskeleton dynamics. To advance our understanding of metastatic cancer dissemination, we have developed a model system that is based on two v-src transformed chicken sarcoma cell lines-the highly metastatic parental PR9692 and a non-metastasizing but fully tumorigenic clonal derivative PR9692-E9. Oligonucleotide microarray analysis of both cell lines revealed that the gene encoding the transcription factor EGR1 was downregulated in the non-metastatic PR9692-E9 cells. Further investigation demonstrated that the introduction of exogenous EGR1 into PR9692-E9 cells restored their metastatic potential to a level indistinguishable from parental PR9692 cells. Microarray analysis of EGR1 reconstituted cells revealed the activation of genes that are crucial for actin cytoskeleton contractility (MYL9), filopodia formation (MYO10), the production of specific extracellular matrix components (HAS2, COL6A1-3) and other essential pro-metastatic abilities.
References provided by Crossref.org
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