Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2005-9-16
pubmed:abstractText
Although a strong correlation between neuroendocrine differentiation and angiogenesis of prostate cancer has been reported, no mechanistic link between the two events has been established. Because neuropeptide calcitonin is secreted by prostate tumors and endothelial cells are known to express calcitonin receptor-like receptor, we examined the potential action of calcitonin on endothelial cells. The presence of calcitonin receptor, calcitonin receptor-like receptor, and receptor activity-modifying proteins in human microvessel endothelial-1 cells was tested by reverse transcriptase-PCR (RT-PCR). The proangiogenic action of calcitonin was examined in several in vitro models of angiogenesis using HMEC-1 cells and also in vivo using dorsal skinfold assays. Calcitonin expression of PC-3M cells was modulated, and its effect on angiogenesis was examined in in vitro as well as in vivo models. The results of RT-PCR and radioligand receptor assays showed the presence of functional calcitonin receptor in HMEC-1 cells. Calcitonin stimulated all phases of angiogenesis through the calcitonin receptor, but its effect on tube morphogenesis by endothelial cells occurred at the concentration of the Kd of calcitonin receptor. Silencing of calcitonin receptor expression in HMEC-1 cells abolished calcitonin-induced tube formation. Vascular endothelial growth factor antibodies attenuated but did not abolish calcitonin-induced tube morphogenesis. PC-3M prostate cancer cells induced angiogenesis in in vivo and in vitro models. Overexpression of calcitonin in PC-3M cells increased their angiogenic activity, whereas the silencing of calcitonin expression abolished it. These results show that prostate tumor-derived calcitonin may play an important role in prostate tumor growth by regulating intratumoral vascularization.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/CALCRL protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Calcitonin, http://linkedlifedata.com/resource/pubmed/chemical/Calcitonin Receptor-Like Protein, http://linkedlifedata.com/resource/pubmed/chemical/Calcrl protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Collagen, http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary, http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations, http://linkedlifedata.com/resource/pubmed/chemical/Laminin, http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Calcitonin, http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A, http://linkedlifedata.com/resource/pubmed/chemical/matrigel
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
65
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8519-29
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16166333-Animals, pubmed-meshheading:16166333-Binding Sites, pubmed-meshheading:16166333-Calcitonin, pubmed-meshheading:16166333-Calcitonin Receptor-Like Protein, pubmed-meshheading:16166333-Cell Growth Processes, pubmed-meshheading:16166333-Cell Movement, pubmed-meshheading:16166333-Collagen, pubmed-meshheading:16166333-DNA, Complementary, pubmed-meshheading:16166333-Drug Combinations, pubmed-meshheading:16166333-Endothelial Cells, pubmed-meshheading:16166333-Humans, pubmed-meshheading:16166333-Laminin, pubmed-meshheading:16166333-Mice, pubmed-meshheading:16166333-Mice, Nude, pubmed-meshheading:16166333-Neovascularization, Physiologic, pubmed-meshheading:16166333-Proteoglycans, pubmed-meshheading:16166333-Receptors, Calcitonin, pubmed-meshheading:16166333-Skin, pubmed-meshheading:16166333-Stimulation, Chemical, pubmed-meshheading:16166333-Vascular Endothelial Growth Factor A
pubmed:year
2005
pubmed:articleTitle
Calcitonin stimulates multiple stages of angiogenesis by directly acting on endothelial cells.
pubmed:affiliation
Department of Pharmacology, University of Louisiana School of Pharmacy, College of Health Sciences, Monroe, Louisiana 71209, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural