Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2004-3-18
pubmed:abstractText
Papillary thyroid carcinomas are characterized by rearrangements of the RET receptor tyrosine kinase generating RET/PTC oncogenes. Here we show that osteopontin (OPN), a secreted glycoprotein, is a major RET/PTC-induced transcriptional target in PC Cl 3 thyroid follicular cells. OPN upregulation depended on the integrity of the RET/PTC kinase and tyrosines Y1015 and Y1062, two major RET/PTC autophosphorylation sites. RET/PTC also induced a strong overexpression of CD44, a cell surface signalling receptor for OPN. Upregulation of CD44 was dependent on RET/PTC Y1062, as well. Constitutive OPN overexpression or treatment with exogenous recombinant OPN sharply increased proliferation, Matrigel invasion and spreading in collagen gels of RET/PTC-transformed PC Cl 3 cells. These effects were impaired by the treatment of PC Cl 3-RET/PTC cells with OPN- and CD44-locking antibodies. Thus, RET/PTC signalling triggers an autocrine loop involving OPN and CD44 that sustains proliferation and invasion of transfomed PC Cl 3 thyrocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD44, http://linkedlifedata.com/resource/pubmed/chemical/Collagen, http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type I, http://linkedlifedata.com/resource/pubmed/chemical/DNA, http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations, http://linkedlifedata.com/resource/pubmed/chemical/Laminin, http://linkedlifedata.com/resource/pubmed/chemical/Osteopontin, http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Receptor Protein-Tyrosine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins, http://linkedlifedata.com/resource/pubmed/chemical/SPP1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Sialoglycoproteins, http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine, http://linkedlifedata.com/resource/pubmed/chemical/matrigel
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2188-96
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:14981541-Antigens, CD44, pubmed-meshheading:14981541-Carcinoma, Papillary, pubmed-meshheading:14981541-Cell Division, pubmed-meshheading:14981541-Cell Line, Tumor, pubmed-meshheading:14981541-Cell Transformation, Neoplastic, pubmed-meshheading:14981541-Collagen, pubmed-meshheading:14981541-Collagen Type I, pubmed-meshheading:14981541-DNA, pubmed-meshheading:14981541-Drug Combinations, pubmed-meshheading:14981541-Gene Expression Regulation, Neoplastic, pubmed-meshheading:14981541-Humans, pubmed-meshheading:14981541-Laminin, pubmed-meshheading:14981541-Neoplasm Invasiveness, pubmed-meshheading:14981541-Osteopontin, pubmed-meshheading:14981541-Phenotype, pubmed-meshheading:14981541-Phosphorylation, pubmed-meshheading:14981541-Protein Structure, Tertiary, pubmed-meshheading:14981541-Proteoglycans, pubmed-meshheading:14981541-Proto-Oncogene Proteins, pubmed-meshheading:14981541-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:14981541-Recombinant Proteins, pubmed-meshheading:14981541-Sialoglycoproteins, pubmed-meshheading:14981541-Signal Transduction, pubmed-meshheading:14981541-Thyroid Neoplasms, pubmed-meshheading:14981541-Tyrosine
pubmed:year
2004
pubmed:articleTitle
Autocrine stimulation by osteopontin plays a pivotal role in the expression of the mitogenic and invasive phenotype of RET/PTC-transformed thyroid cells.
pubmed:affiliation
Dipartimento di Biologia e Patologia Cellulare e Molecolare, University Federico II c/o Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, Naples, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't