Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-12-30
pubmed:abstractText
Chondrosarcoma is a type of highly malignant tumour with a potent capacity to invade locally and cause distant metastasis. Chondrosarcoma shows a predilection for metastasis to the lungs. Tumour necrosis factor (TNF)-? is a key cytokine involved in inflammation, immunity, cellular homeostasis and tumour progression. Integrins are the major adhesive molecules in mammalian cells and have been associated with metastasis of cancer cells. However, the effects of TNF-? in migration and integrin expression in chondrosarcoma cells are largely unknown. In this study, we found that TNF-? increased the migration and the expression of ?v?3 integrin in human chondrosarcoma cells. Activations of MAPK kinase (MEK), extracellular signal-regulating kinase (ERK) and nuclear factor-?B (NF-?B) pathways after TNF-? treatment were demonstrated, and TNF-?-induced expression of integrin and migration activity was inhibited by the specific inhibitor and mutant of MEK, ERK and NF-?B cascades. Taken together, our results indicated that TNF-? enhances the migration of chondrosarcoma cells by increasing ?v?3 integrin expression through the MEK/ERK/NF-?B signal transduction pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1097-4652
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
226
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
792-9
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
TNF-? increases ?v?3 integrin expression and migration in human chondrosarcoma cells.
pubmed:affiliation
Department of Orthopedic Surgery, National Taiwan University Hospital, and Institute of Biomedical Engineering, College of Medicine, National Taiwan University, Taipei, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't