Linked Life Data

7529189

Source:http://linkedlifedata.com/resource/pubmed/id/7529189

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-2-9
pubmed:abstractText
Some human neoplasms show aberrant expression or overexpression of epidermal growth factor (EGF) receptor, and the degree of the receptor expression is correlated with the malignant phenotype in certain epithelial tumors including squamous carcinoma cells. Since phenotypic transformation of cells could involve quantitative and qualitative alteration of integrin function, the effects of EGF on cell-matrix interactions were studied using HSC-1 cells, a human squamous carcinoma cell line showing EGF receptor overexpression. The EGF-treated HSC-1 cells interacted with matrix proteins differently from the untreated cells, as shown by cell adhesion and phagokinetic track assays. Among fibronectin, laminin, fibrinogen, and type I collagen, fibronectin was the most efficient substratum to promote untreated HSC-1 cell adhesion and migration. Pretreatment of the cells with 50 ng/ml EGF for 18 h selectively increased the number of spread cells and the size of the individual cell migration area on type I collagen by 250 and 400%, respectively. The same pretreatment diminished cell adhesion and migration on other substrata so that the EGF treatment converted type I collagen as the most efficient substratum for cell adhesion and migration of the HSC-1 cells. ELISA and immunoprecipitation studies showed that EGF up-regulated the expression of alpha 2 beta 1 integrin collagen receptor in a time- and dose-dependent manner by stimulating biosynthesis of alpha 2 subunit, but did not up-regulate those of the alpha 3 beta 1, alpha 5 beta 1, or alpha v beta 3 integrins. These results suggest that EGF preferentially enhances HSC-1 cell interaction with type I collagen, leading to the enhanced cellular migratory activity on the substratum, as a result of selective up-regulation of alpha 2 beta 1 integrin expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0014-4827
pubmed:author
pubmed:issnType
Print
pubmed:volume
216
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
261-72
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:7529189-Antigens, CD, pubmed-meshheading:7529189-Antigens, CD29, pubmed-meshheading:7529189-Antineoplastic Agents, pubmed-meshheading:7529189-Carcinoma, Squamous Cell, pubmed-meshheading:7529189-Cell Adhesion, pubmed-meshheading:7529189-Cell Movement, pubmed-meshheading:7529189-Collagen, pubmed-meshheading:7529189-Epidermal Growth Factor, pubmed-meshheading:7529189-Extracellular Matrix Proteins, pubmed-meshheading:7529189-Gene Amplification, pubmed-meshheading:7529189-Gene Expression Regulation, Neoplastic, pubmed-meshheading:7529189-Humans, pubmed-meshheading:7529189-Integrins, pubmed-meshheading:7529189-Oligopeptides, pubmed-meshheading:7529189-Receptor, Epidermal Growth Factor, pubmed-meshheading:7529189-Skin Neoplasms, pubmed-meshheading:7529189-Tumor Cells, Cultured, pubmed-meshheading:7529189-Up-Regulation
pubmed:year
1995
pubmed:articleTitle
Epidermal growth factor enhancement of HSC-1 human cutaneous squamous carcinoma cell adhesion and migration on type I collagen involves selective up-regulation of alpha 2 beta 1 integrin expression.
pubmed:affiliation
Department of Dermatology, Kobe City General Hospital, Japan.
pubmed:publicationType
Journal Article