Linked Life Data

12063543

Source:http://linkedlifedata.com/resource/pubmed/id/12063543

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-6-13
pubmed:abstractText
Overexpression of the epidermal growth factor receptor (EGFR) is thought to play a key role in the development of head and neck squamous cell carcinoma (HNSCC) primarily through its effect on promoting uncontrolled cell proliferation. Blocking EGFR ligand binding might also inhibit angiogenesis and down-regulate the production of angiogenic factors. Angiogenesis is increased in various human tumors, including head and neck squamous cell carcinoma (HNSCC), and correlates with tumor progression and metastasis. The vascular endothelial growth factor (VEGF) is thought to be the most important angiogenic factor. We determined whether VEGF antisense oligonucleotide treatment can decrease angiogenic activity of HNSCC cell lines in vitro. By using a 21-mer antisense phosphorothioate oligonucleotide targeting the translation start site of human EGFR mRNA, we examined modulation of VEGF expression in cell line supernatants by capture ELISA, and in cell lysates by Western blotting. Human umbilica vein endothelial cells (HUVEC) were grown in conditioned medium produced from the treated tumor cells. Endothelial cell migration was measured using a modified Boyden chamber. EGFR antisense oligonucleotide treatment resulted in a significant reduction of VEGF protein expression compared to sense oligonucleotide control. Addition of conditioned medium from EGFR antisense-treated tumor cells resulted in decreased endothelial cell migration. In conclusion, therapeutic strategies targeting EGFR signaling in head and neck cancer might have an antitumor effect mediated in part by inhibition of tumor angiogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1019-6439
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
11-6
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12063543-Carcinoma, Squamous Cell, pubmed-meshheading:12063543-Cell Movement, pubmed-meshheading:12063543-Down-Regulation, pubmed-meshheading:12063543-Endothelial Growth Factors, pubmed-meshheading:12063543-Endothelium, Vascular, pubmed-meshheading:12063543-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:12063543-Head and Neck Neoplasms, pubmed-meshheading:12063543-Humans, pubmed-meshheading:12063543-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:12063543-Lymphokines, pubmed-meshheading:12063543-Oligonucleotides, Antisense, pubmed-meshheading:12063543-Receptor, Epidermal Growth Factor, pubmed-meshheading:12063543-Tumor Cells, Cultured, pubmed-meshheading:12063543-Vascular Endothelial Growth Factor A, pubmed-meshheading:12063543-Vascular Endothelial Growth Factors
pubmed:year
2002
pubmed:articleTitle
EGFR antisense treatment of human HNSCC cell lines down-regulates VEGF expression and endothelial cell migration.
pubmed:affiliation
Univ.-HNO-Klinik, Klinikum, Theodor-Kutzer-Ufer, D-68135 Mannheim, Germany. frank.riedel@hno.ma.uni-heidelberg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't