Suppression of tumorigenicity in Ras-transformed fibroblasts by alpha 2(I) collagen.

2.50
Hdl Handle:
http://hdl.handle.net/10541/95515
Title:
Suppression of tumorigenicity in Ras-transformed fibroblasts by alpha 2(I) collagen.
Authors:
Travers, H; French, Neil S; Norton, John D
Abstract:
Transformed fibroblasts exhibit reduced adhesion to substrata, a characteristic attributable in part to reduced expression/increased degradation of extracellular matrix (EM) proteins such as type I collagen. To directly assess the role of EM proteins in cellular transformation, a vKRas-transformed mouse fibroblast cell line was transfected with an alpha 2(I) collagen expression construct. Stable transfectants displaying a partial restoration of type I collagen expression showed a flatter morphology with increased adherence to the substratum. These clones also exhibited a reduced ability to clone in soft agar, slower growth kinetics, and suppression of tumorigenicity in nude mice. Restoration of type I collagen is correlated with down-regulation of ras oncogene-responsive NVL3 VL30 gene expression. These results suggest that in addition to suppressing tumorigenicity by promoting cellular adhesion and cytoskeletal organization, EM proteins such as type I collagen may also act to subvert oncoprotein signaling pathways associated with the malignant phenotype.
Affiliation:
Cancer Research Campaign, Department of Gene Regulation, Paterson Institute for Cancer Research, Christie Hospital National Health Service Trust, Manchester, United Kingdom.
Citation:
Suppression of tumorigenicity in Ras-transformed fibroblasts by alpha 2(I) collagen. 1996, 7 (10):1353-60 Cell Growth Differ.
Journal:
Cell Growth & Differentiation
Issue Date:
Oct-1996
URI:
http://hdl.handle.net/10541/95515
PubMed ID:
8891339
Type:
Article
Language:
en
ISSN:
1044-9523
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
dc.contributor.authorTravers, Hen
dc.contributor.authorFrench, Neil Sen
dc.contributor.authorNorton, John Den
dc.date.accessioned2010-04-01T15:05:10Z-
dc.date.available2010-04-01T15:05:10Z-
dc.date.issued1996-10-
dc.identifier.citationSuppression of tumorigenicity in Ras-transformed fibroblasts by alpha 2(I) collagen. 1996, 7 (10):1353-60 Cell Growth Differ.en
dc.identifier.issn1044-9523-
dc.identifier.pmid8891339-
dc.identifier.urihttp://hdl.handle.net/10541/95515-
dc.description.abstractTransformed fibroblasts exhibit reduced adhesion to substrata, a characteristic attributable in part to reduced expression/increased degradation of extracellular matrix (EM) proteins such as type I collagen. To directly assess the role of EM proteins in cellular transformation, a vKRas-transformed mouse fibroblast cell line was transfected with an alpha 2(I) collagen expression construct. Stable transfectants displaying a partial restoration of type I collagen expression showed a flatter morphology with increased adherence to the substratum. These clones also exhibited a reduced ability to clone in soft agar, slower growth kinetics, and suppression of tumorigenicity in nude mice. Restoration of type I collagen is correlated with down-regulation of ras oncogene-responsive NVL3 VL30 gene expression. These results suggest that in addition to suppressing tumorigenicity by promoting cellular adhesion and cytoskeletal organization, EM proteins such as type I collagen may also act to subvert oncoprotein signaling pathways associated with the malignant phenotype.en
dc.language.isoenen
dc.subject.mesh3T3 Cells-
dc.subject.meshAnimals-
dc.subject.meshCell Adhesion-
dc.subject.meshCell Division-
dc.subject.meshCell Transformation, Neoplastic-
dc.subject.meshCollagen-
dc.subject.meshGene Expression Regulation, Neoplastic-
dc.subject.meshGenes, ras-
dc.subject.meshMice-
dc.subject.meshSignal Transduction-
dc.titleSuppression of tumorigenicity in Ras-transformed fibroblasts by alpha 2(I) collagen.en
dc.typeArticleen
dc.contributor.departmentCancer Research Campaign, Department of Gene Regulation, Paterson Institute for Cancer Research, Christie Hospital National Health Service Trust, Manchester, United Kingdom.en
dc.identifier.journalCell Growth & Differentiationen
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