Linked Life Data

11034115

Source:http://linkedlifedata.com/resource/pubmed/id/11034115

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-1-11
pubmed:abstractText
Melatonin, a pineal secretory product, has been shown to exert a direct anti-proliferative action on the androgen-sensitive LNCaP prostate cancer cell line through hitherto undefined mechanisms. In this communication, expression of mt1 melatonin receptor protein in human prostate cancer tissues and LNCaP cells was demonstrated by immunohisto(cyto)chemistry and western blotting, hence supporting the use of LNCaP cell line as a model for the study of melatonin signaling in prostate cancer cell growth. Using 3H-thymidine incorporation assay, LNCaP cell proliferation was inhibited by 2-iodomelatonin, a high-affinity melatonin receptor agonist. Furthermore, melatonin inhibited 3H-thymidine incorporation into LNCaP cells and attenuated 5alpha-dihydrotestosterone (DHT) or 17beta-estradiol (E2)-induced stimulation of LNCaP cell proliferation at physiological and pharmacological concentrations. Similar concentration-dependent inhibition of sex steroid-induced stimulation of thymidine incorporation into LNCaP cells by 2-iodomelatonin was also observed. Interestingly, attenuation of sex steroid-stimulated calcium influx into LNCaP cells by pharmacological concentrations of melatonin was recorded, whereas 2-iodomelatonin had no effect on cytosolic calcium changes induced by sex steroids. In addition, proliferative and cytosolic calcium changes were associated with inhibition of total prostate-specific antigen (PSA) production by LNCaP cells at high physiological and pharmacological concentrations of melatonin. Our data suggest that activated mt1 receptor and attenuated sex steroid-induced calcium influx are two important mechanisms mediating the direct anti-proliferative action of melatonin on androgen-responsive human prostate cancer cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0742-3098
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
172-83
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11034115-Adenocarcinoma, pubmed-meshheading:11034115-Blotting, Western, pubmed-meshheading:11034115-Calcium, pubmed-meshheading:11034115-Cell Division, pubmed-meshheading:11034115-Dihydrotestosterone, pubmed-meshheading:11034115-Dose-Response Relationship, Drug, pubmed-meshheading:11034115-Estradiol, pubmed-meshheading:11034115-Humans, pubmed-meshheading:11034115-Immunoenzyme Techniques, pubmed-meshheading:11034115-Male, pubmed-meshheading:11034115-Melatonin, pubmed-meshheading:11034115-Neoplasms, Hormone-Dependent, pubmed-meshheading:11034115-Prostatic Neoplasms, pubmed-meshheading:11034115-RNA, Messenger, pubmed-meshheading:11034115-Receptors, Cell Surface, pubmed-meshheading:11034115-Receptors, Cytoplasmic and Nuclear, pubmed-meshheading:11034115-Receptors, Melatonin, pubmed-meshheading:11034115-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11034115-Tumor Cells, Cultured
pubmed:year
2000
pubmed:articleTitle
Potential involvement of mt1 receptor and attenuated sex steroid-induced calcium influx in the direct anti-proliferative action of melatonin on androgen-responsive LNCaP human prostate cancer cells.
pubmed:affiliation
Department of Physiology, Faculty of Medicine, The University of Hong Kong, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't