Document Detail

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.
MedLine Citation:
PMID:  11034115     Owner:  NLM     Status:  MEDLINE    
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.
S C Xi; P C Tam; G M Brown; S F Pang; S Y Shiu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of pineal research     Volume:  29     ISSN:  0742-3098     ISO Abbreviation:  J. Pineal Res.     Publication Date:  2000 Oct 
Date Detail:
Created Date:  2001-01-11     Completed Date:  2001-01-25     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8504412     Medline TA:  J Pineal Res     Country:  DENMARK    
Other Details:
Languages:  eng     Pagination:  172-83     Citation Subset:  IM    
Department of Physiology, Faculty of Medicine, The University of Hong Kong, China.
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MeSH Terms
Adenocarcinoma / drug therapy,  metabolism*,  pathology
Blotting, Western
Calcium / metabolism*
Cell Division / drug effects*
Dihydrotestosterone / pharmacology
Dose-Response Relationship, Drug
Estradiol / pharmacology
Immunoenzyme Techniques
Melatonin / analogs & derivatives*,  pharmacology*
Neoplasms, Hormone-Dependent / drug therapy,  metabolism*,  pathology
Prostatic Neoplasms / drug therapy,  metabolism*,  pathology
RNA, Messenger / metabolism
Receptors, Cell Surface / genetics,  metabolism*
Receptors, Cytoplasmic and Nuclear / genetics,  metabolism*
Receptors, Melatonin
Reverse Transcriptase Polymerase Chain Reaction
Tumor Cells, Cultured / drug effects,  metabolism
Reg. No./Substance:
0/RNA, Messenger; 0/Receptors, Cell Surface; 0/Receptors, Cytoplasmic and Nuclear; 0/Receptors, Melatonin; 50-28-2/Estradiol; 521-18-6/Dihydrotestosterone; 73-31-4/Melatonin; 7440-70-2/Calcium; 93515-00-5/2-iodomelatonin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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